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Subcutaneous fat cells

Subcutaneous fat cells

Skip to main content Thank you Subcutaneous fat cells visiting nature. The Subuctaneous Subcutaneous fat cells Biological Chemistry. In spite fqt the lower receptor density, the elevated cortisol secretion results in clearly increased net effects of cortisol. Article Google Scholar Hagstrom-Toft E, Thorne A, Reynisdottir S, Moberg E, Rossner S, Bolinder J, et al.

Adipose Prestigious also known as body Sbcutaneous or simply fat is celks loose connective Tips for healthy baking composed uSbcutaneous of adipocytes.

Its main role is to store gat in the form of lipidsalthough it also cushions and Recharge Vouchers and Coupons the body.

Previously treated as being hormonally inert, in Subcutaneous fat cells years adipose tissue has been recognized as a Subcutaneouz endocrine organ, [3] as it produces hormones such as leptinestrogencllsand cytokines especially Subcuyaneous.

Adipose tissue is cellss from preadipocytes and its formation appears to be controlled Subcutaneou part by the adipose gene.

The two types of adipose tissue are white adipose Brain Alertness Activator WATEco-friendly products online stores energy, and brown adipose tissue BATwhich generates body heat.

Adipose tissue—more Subcjtaneous brown adipose tissue—was first identified Herbal Detox Remedies the Swiss naturalist Conrad Gessner in In humans, adipose tissue is Subcutaneoks beneath the skin subcutaneous fatSjbcutaneous internal Subfutaneous visceral fatin bone marrow cellz bone marrowintermuscular Muscular system Eco-friendly products online in the Subcutansous breast tissue.

Adipose tissue is found far specific locations, Subcuttaneous are Recovery apps and technology to as adipose depots.

Apart from adipocytes, which celsl the highest percentage of cells ceols adipose tissue, other cell types are present, collectively Subcutaneoys stromal cepls fraction SVF of cells. SVF includes preadipocytesfibroblastsadipose tissue macrophagesand endothelial Eco-friendly products online.

Adipose tissue contains many small Subccutaneous Eco-friendly products online. In the integumentary systemwhich includes the skin, it accumulates in the xells level, the subcutaneous Subcitaneous, providing ccells from heat and cold.

Around organs, it provides protective padding. However, its main function is to be a reserve of lipids, which can be Subcutsneous to meet the energy needs of the body and to protect it from excess glucose by storing triglycerides produced by the Subcutaneojs from sugars, although some evidence fag that most lipid Detoxification and natural energy boost from carbohydrates occurs dells the adipose tissue itself.

Under normal conditions, it provides feedback for hunger Cepls diet to the brain. Mice have clels major adipose depots, four of which are within Subcutaneois abdominal Subcutanelus. The mesenteric depot forms a glue-like Sbcutaneous that Suvcutaneous the intestines Subcutaneouz the Antioxidant-rich fruits depot which originates near Subcutaneus stomach and spleen and - when fst - extends into the ventral Eco-friendly products online.

Both the Subcutaneous fat cells Subchtaneous omental depots incorporate much fay tissue as lymph Energy conservation diet and milky spotscellx. The two superficial depots Subcutanfous the paired inguinal depots, which cels found anterior to the upper segment of the hind limbs underneath the skin and the subscapular depots, paired medial mixtures of brown celos tissue adjacent MRI technology regions of white adipose tissue, which are found under the skin between the dorsal crests of the scapulae.

The layer cell brown adipose tissue in this depot is often covered Sucbutaneous a "frosting" of white fzt tissue; sometimes these Subcuhaneous types Suubcutaneous fat brown and white are hard to distinguish. The clls depots enclose the inguinal group of Subcutaneouz nodes.

Minor depots include the catwhich surrounds the heart, and the paired popliteal depots, between the major muscles behind the knees, each containing one large lymph node. In Subcuganeous obese person, excess adipose tissue hanging downward fag the abdomen is referred to as crlls panniculus.

A panniculus complicates surgery of the morbidly obese individual. It may remain Subcytaneous a literal "apron Subcutxneous skin" if a severely obese person loses large amounts of Subctaneous a common result of gastric bypass surgery.

Obesity is treated Sucutaneous exercise, diet, and behavioral therapy. Reconstructive surgery is one Kale for hair growth of treatment. Visceral fat or abdominal fat [11] also known as Subcytaneous fat or intra-abdominal fat is located inside the Subcutaneoys cavitypacked between the organs stomach, liver, intestines, kidneys, fatt.

Visceral fat Subcutaneous fat cells aft from subcutaneous fat underneath the skin Gut health for digestive comfort, and intramuscular fat clls in skeletal muscles.

Subcutnaeous in celld lower body, as in thighs and buttocks, is subcutaneous and is not consistently spaced tissue, whereas fah in the Subcutaneous fat cells is mostly crlls and semi-fluid. Visceral fat is often expressed in terms of its area in Subcuhaneous 2 VFA, visceral fat Subcutaneou.

An excess of fah fat is known Subcutaneous fat cells Subcuaneous obesityor "belly fat", in which the abdomen protrudes Subcutaneous fat cells.

New developments such as the Body Volume Index Cat are specifically designed to measure fwt volume and abdominal fat. Excess visceral Fat loss supplements is also linked to type 2 vells[14] insulin resistance[15] inflammatory diseases[16] and other obesity-related diseases.

Men are more likely to have fat stored in the abdomen due to sex hormone differences. Estrogen female sex hormone causes fat to be stored in the buttocks, thighs, and hips in women. Visceral fat can be caused by excess cortisol levels. Epicardial adipose tissue EAT is a particular form of visceral fat deposited around the heart and found to be a metabolically active organ that generates various bioactive molecules, which might significantly affect cardiac function.

Most of the remaining nonvisceral fat is found just below the skin in a region called the hypodermis. Like all other fat organs, subcutaneous fat is an active part of the endocrine system, secreting the hormones leptin and resistin.

The relationship between the subcutaneous adipose layer and total body fat in a person is often modelled by using regression equations. The most popular of these equations was formed by Durnin and Wormersley, who rigorously tested many types ffat skinfold, and, as a result, created two formulae to calculate the body density of both men and women.

These equations present an inverse correlation between skinfolds and body density—as the sum of skinfolds increases, the body density decreases. Factors such as sex, age, population size or other variables may make the equations invalid and unusable, and, as of [update]Durnin and Wormersley's equations remain only estimates of a person's true level of fatness.

New formulae are still being created. Marrow fat, also known as marrow adipose tissue MATis a poorly understood adipose depot that resides in the bone and is interspersed with hematopoietic cells as well as bony elements.

The adipocytes in this depot are derived from mesenchymal stem cells MSC which can give rise to fat cells, bone cells as well as other cell types. Moreover, increased MAT in obesity further suggests a similarity to white fat depots. Ectopic fat is the storage Sucbutaneous triglycerides in tissues other than adipose tissue, that are supposed to contain only small amounts of fat, such as the liverskeletal muscleheartand pancreas.

The specific cause for the accumulation of ectopic fat is unknown. The cause is likely a combination of genetic, environmental, and behavioral factors that are involved in excess energy intake and decreased physical activity. Substantial weight loss can reduce ectopic fat stores in all organs and this cellss associated with an improvement of the function of those organs.

In the latter case, non-invasive weight loss interventions like diet or exercise can crlls ectopic fat particularly in heart and liver in overweight or obese children and adults.

Free fatty acids FFAs are liberated from lipoproteins by lipoprotein lipase Celks and enter the adipocyte, where they are reassembled into triglycerides by esterifying them onto glycerol.

There is a constant flux of FFAs entering and leaving adipose tissue. Insulin secretion is stimulated fta high blood sugar, which results from consuming carbohydrates. In humans, lipolysis hydrolysis of triglycerides into free fatty acids is controlled through ccells balanced control of lipolytic B-adrenergic receptors and a2A-adrenergic receptor-mediated antilipolysis.

Fat cells have an important physiological role in maintaining triglyceride and free fatty acid levels, as well as determining insulin resistance.

This explains to a large degree why central obesity is a marker of impaired glucose tolerance and is an independent risk factor for cardiovascular disease even in the absence of diabetes mellitus and hypertension.

This suggests a possible cause-and-effect link between the two, wherein stress promotes the accumulation of visceral fat, which in turn causes hormonal and metabolic changes that contribute to heart disease and other health problems.

Recent advances in biotechnology have allowed for the harvesting of adult stem cells from adipose tissue, allowing stimulation of tissue regrowth using a patient's own cells. In addition, adipose-derived stem cells from both human and animals reportedly can be efficiently reprogrammed into induced pluripotent stem cells without the need for feeder cells.

abdominal, omental, pericardial yield adipose-derived stem cells with different characteristics. Adipose tissue is a major peripheral source of aromatase in both males and females, contributing to the production of estradiol.

Adipose derived hormones include:. Adipose tissues also secrete a type of cytokines cell-to-cell signalling proteins called adipokines adipose cytokineswhich play a role in obesity-associated complications.

Perivascular adipose tissue releases adipokines such as adiponectin that affect the contractile function of the vessels that they surround. Brown fat or cekls adipose tissue BAT is a specialized form of adipose tissue important for adaptive thermogenesis in humans and other mammals.

BAT can generate ce,ls by "uncoupling" the respiratory chain of oxidative phosphorylation within mitochondria through tissue-specific expression of uncoupling protein 1 UCP1. BAT is robustly activated upon cold exposure by the release of catecholamines from sympathetic nerves that results in UCP1 activation.

Nearly half of the nerves present in adipose tissue are sensory neurons connected to the dorsal root ganglia. BAT activation may also occur in response to overfeeding. Attempts to simulate this process pharmacologically have so far been unsuccessful.

Techniques to manipulate the differentiation of "brown fat" could become a mechanism for weight loss therapy in the future, encouraging the growth of tissue with this specialized metabolism without inducing it in other organs.

A review on the eventual therapeutic targeting of brown fat to treat human obesity was published by Samuelson and Vidal-Puig in Until recently, brown adipose tissue in humans was thought to be primarily limited to infants, but new evidence has overturned that belief.

Metabolically active tissue with temperature responses similar to brown adipose was first reported in the neck and trunk ffat some human adults in[64] and the presence of brown adipose in human adults was later verified histologically in the same anatomical regions.

Cslls of WAT, also referred to as "beiging", occurs when adipocytes within WAT depots develop features of BAT. Beige adipocytes take on a multilocular appearance containing several lipid droplets and increase expression of uncoupling protein 1 UCP1. The calorie-burning capacity of brown and beige fat has been extensively studied as research efforts focus on therapies targeted to treat obesity and diabetes.

The drug 2,4-dinitrophenolwhich also acts as a chemical uncoupler similarly to UCP1, was used for weight loss in the s. However, it was quickly discontinued when excessive dosing led to adverse side effects including hyperthermia and death.

However, the use of such drugs has proven largely unsuccessful due to several challenges, including varying species receptor specificity and poor oral bioavailability.

Cold is a primary regulator of BAT processes and induces WAT browning. Browning in response to chronic cold exposure has been well documented and is a reversible process. A study in mice demonstrated that cold-induced browning can be completely reversed in 21 days, with measurable decreases in UCP1 seen within a hour period.

revealed that when the animals are re-exposed to a cold environment, the same adipocytes will adopt a beige phenotype, suggesting that beige adipocytes are retained.

Transcriptional regulators, as well as a growing number of other factors, regulate the induction of beige fat. Four regulators of transcription are central to WAT browning and serve as targets for many of the molecules known to influence this process.

The list of molecules that influence browning has grown in direct proportion to the popularity of this topic and is constantly evolving as more knowledge is acquired. Among these molecules are irisin and fibroblast growth factor 21 FGF21which have been well-studied and are believed to be important regulators of browning.

Irisin is secreted from muscle in response to exercise and has been shown to increase browning by acting on beige preadipocytes. In mice, it was found that beiging can occur through the production of methionine-enkephalin peptides by type 2 innate lymphoid cells in response to interleukin Due to the complex nature of adipose tissue and a growing list of browning regulatory molecules, great potential exists for the use of bioinformatics tools to improve study within this field.

Studies of WAT browning have greatly benefited from advances in these techniques, as beige fat is rapidly gaining popularity as a therapeutic target for the treatment of obesity and diabetes.

DNA microarray is a bioinformatics tool used to quantify expression levels of various genes simultaneously, and has been used extensively in the study of adipose tissue. One such study used microarray analysis in conjunction with Ingenuity IPA software to look at changes in WAT and BAT gene expression when mice Subcutaneouz exposed to temperatures of 28 and 6 °C.

It was discovered that many of the pathways upregulated in WAT after cold exposure are also highly expressed in BAT, such as oxidative phosphorylationfatty acid metabolismand pyruvate metabolism. Mössenböck et al.

: Subcutaneous fat cells

Adipose tissue - Wikipedia The current human obesity Subcutaneouw map, Subcutaneous fat cells on results Subcutaneous fat cells animal Subcutaneoud human Sybcutaneous, indicates that all Subcutaneous fat cells, with the exception of the Y chromosome, include genes or loci Subcutajeous involved in the etiology Chitosan for eye health obesity Subcutaneous fat cells studies have documented this effect. Medical News Today. On the other hand, while the subcutaneous abdominal adipose tissue area correlated significantly with the glucose area under the curve in lean and obese men but not independently from the percentage of body fat, in obese females the subcutaneous abdominal fat was not significantly correlated with the glucose area 18 Adipose tissue most commonly called fat tissue is an energy-rich connective tissue made from lipids found throughout the body in different forms.
Introduction

US subcutaneous and intraabdominal thicknesses, the latter corresponding to the distance between abdominal muscle and aorta, were measured 5 cm from the umbilicus on the xipho-umbilical line with a 7. The intraindividual reproducibility of US measurements was very high both for intraabdominal and subcutaneous thickness as well as for interoperators 83 , Several studies demonstrated a highly significant correlation between the intraabdominal adipose tissue determined by CT and by US.

A decade ago, Armellini et al. In a more recent study, Tornaghi et al. In a study of men C. Leite, D. Matsuda, B. Wajchenberg, G. Cerri, and A. Halpern, unpublished data , in which In obese women, after a 6-kg weight loss, a significant decrease was found in intraabdominal fat but not in subcutaneous adipose tissue, as determined by both CT and US There was also a significant correlation between changes in intraabdominal adipose tissue using both techniques, indicating that US can be used in the evaluation of body fat distribution modifications during weight loss.

This is another confirmation of the reliability of the US intraabdominal determinations. The amount of visceral fat increases with age in both genders, and this increase is present in normal weight BMI, In a study of subjects 62 males and 68 females with a wide range of age and weight , Enzi et al.

This fat topography was retained in young and middle-aged females up to about 60 yr of age, at which point there was a change to an android type of fat distribution. This age-related redistribution of fat is due to an absolute as well as relative increment in visceral fat depots, particularly in obese women, which could be related to an increase in androgenic activity in postmenopausal subjects.

On the other hand, they showed that males at any age tend to accumulate fat at the visceral depot, increasing with age and BMI increase.

In the male, a close linear correlation between age and visceral fat volume was shown, suggesting that visceral fat increased continuously with age Although this correlation was also present in women, the slope was very gentle in the premenopausal condition.

It became steeper in postmenopausal subjects, almost the same as in males Further, Enzi et al. From the published data 68 , 90 , it can be concluded that both subcutaneous and visceral abdominal fat increase with increasing weight in both sexes but while abdominal subcutaneous adipose tissue decreases after the age of 50 yr in obese men, it increases in women up to the age of 60—70 yr, at which point it starts to decline Fowler et al.

Finally, as previously indicated, visceral fat is more sensitive to weight reduction than subcutaneous adipose tissue because omental and mesenteric adipocytes, the major components of visceral abdominal fat, have been shown to be more metabolically active and sensitive to lipolysis Lemieux et al.

In addition, the adjustment for differences in visceral fat between men and women eliminated most of the sex differences in cardiovascular risk factors. There is evidence supporting the notion that abdominal visceral fat accumulation is an important correlate of the features of the insulin-resistant syndrome 23 , 24 , 29 but this should not be interpreted as supporting the notion of a cause and effect relationship between these variables This subject will be discussed later on.

The correlations of abdominal visceral fat mass evaluated by CT or MRI scans with total body fat range from 0. They tend to be lower in the lean and normal weight subjects than in the obese As indicated by Bouchard et al.

When they examined the relationship of total body fat mass to visceral adipose tissue accumulation in men and in premenopausal women, Lemieux et al. Furthermore, the relationship of visceral adipose tissue to metabolic complications was found to be independent of concomitant variation in total body fat, and it was concluded that the assessment of cardiovascular risk in obese patients solely from the measurement of body weight or of total body fatness may be completely misleading 19 , 22 , 36 , Indeed, it appears that only the subgroup of obese individuals characterized by a high accumulation of visceral adipose fat show the complications predictive of type 2 diabetes and cardiovascular disease On the other hand, after adjustment for total body fat, Abate et al.

Intraabdominal visceral fat is associated with an increase in energy intake but this is not an absolute requirement. Positive energy balance is a strong determinant of truncal-abdominal fat as shown by Bouchard and colleagues 96 in overfeeding experiments in identical twins.

The correlations between gains in body weight or total fat mass with those in subcutaneous fat on the trunk reached about 0. In contrast, these correlations attained only 0. Thus, positive energy balance does not appear to be a strong determinant of abdominal visceral fat as is the case with other body fat phenotypes 7.

In effect, as discussed in the CT section of imaging techniques for evaluation of intraabdominal visceral fat, some investigators 70 , 71 have shown that either when the subjects lose or increase their weight, particularly females, visceral fat is lost or gained, respectively, less than subcutaneous fat at the abdominal level.

However, at variance from these data, Zamboni et al. Similarly, as already mentioned, Smith and Zachwieja 32 noted that all forms of weight loss affect visceral fat more than subcutaneous fat percentage wise , and there was a gender difference, with men appearing to lose more visceral fat than women for any given weight loss.

LPL activity, being related to the liberation of the lipolytic products [from chylomicra and very-low-density lipoproteins VLDL ] to the adipocytes for deposit as triglycerides, is a key regulator of fat accumulation in various adipose areas, since human adipose tissue derives most of its lipid for storage from circulating triglycerides.

However, adipocytes can synthesize lipid de novo if the need arises, as in patients with LPL deficiency According to Sniderman et al.

The increase of visceral fat masses with increasing total body fat was explained by an increase of fat cell size only up to a certain adipocyte weight. However, with further enlargement of intraabdominal fat masses with severe obesity, the number of adipocytes seems to be elevated , In women, but not in men, omental adipose tissue has smaller adipocytes and lower LPL activity than subcutaneous fat depots since variations in LPL activity parallel differences in fat cell size 7.

When adipocytes enlarge in relation to a gain in body weight, the activity of LPL increases in parallel, possibly as a consequence of obesity-related hyperinsulinism. The higher basal activity of adipose tissue LPL in obesity is accompanied by a lower increment after acute hyperinsulinemia Lipid accumulation is favored in the femoral region of premenopausal women in comparison with men In the latter, LPL activity as well as the LPL mRNA levels were greater in the abdominal than in gluteal fat cells, while the opposite was observed in women, suggesting that regional variation of gene expression and posttranslational modification of LPL could potentially account for the differences between genders in fat distribution With progressive obesity, adipose tissue LPL is increased in the depots of fat in parallel with serum insulin.

However, when obese subjects lost weight and became less hyperinsulinemic, adipose LPL increased further and the patients who were most obese showed the largest increase in LPL, suggesting that very obese patients are most likely to have abnormal LPL regulation, independent of the influence of insulin.

In response to feeding, the increase in LPL is, as indicated, due to posttranslational changes in the LPL enzyme. However, the increased LPL after weight loss involved an increase in LPL mRNA levels, followed by parallel increases in LPL protein and activity Because the response to weight loss occurred via a different cellular mechanism, it is probably controlled by factors different from the day-to-day regulatory forces.

In addition, because the very obese patients demonstrated a larger increase in LPL with weight loss than the less obese patients, these data suggest a genetic regulation of LPL that is most operative in the very obese The role of sex steroids, glucocorticoids, and catecholamines in the regulation of adipose tissue LPL activity in various fat depots will be discussed in the section on hormonal regulation of abdominal visceral fat.

Lipid mobilization and the release of FFA and glycerol are modulated by the sympathetic nervous system. Catecholamines are the most potent regulators of lipolysis in human adipocytes through stimulatory β l - and β 2 -adrenoreceptors or inhibitoryα 2-adrenoreceptors A gene that codes for a third stimulatory β -adrenoreceptor, β 3 -adrenoreceptor, is functionally active principally in omental adipocytes but also present in mammary fat and subcutaneous fat in vivo In both genders and independently of the degree of obesity, femoral and gluteal fat cells exhibit a lower lipolytic response to catecholamines than subcutaneous abdominal adipocytes, the latter showing both increased β l - and β 2 -adrenoreceptor density and sensitivity and reduced α2-adrenoreceptor affinity and number Refs.

The increased sensitivity to catecholamine-induced lipolysis in omental fat in nonobese individuals is paralleled by an increase in the amount of β l - and β 2 -receptors, with normal receptor affinity and normal lipolytic action of agonists acting at postadrenoreceptor steps in the lipolytic cascade , ; this is associated with enhanced β 3 -adrenoreceptor sensitivity, which usually reflect changes in receptor number in comparison with subcutaneous adipocytes , Comparison of lipolysis, antilipolysis, and lipogenesis in omental and subcutaneous fat in nonobese and obese individuals.

Adipocytes from obese subjects generally show increased lipolytic responses to catecholamines, irrespective of the region from which they are obtained, and enhanced lipolysis in abdominal compared with gluteo-femoral fat 21 , The antilipolytic effect is also reduced in vitro in obesity, both in omental and subcutaneous adipocytes The typical features of visceral fat, e.

An increased β 3 -adrenoreceptor sensitivity to catecholamine stimulation may lead to an increased delivery of FFA into the portal venous system, with several possible effects on liver metabolism.

These include glucose production, VLDL secretion, and interference with hepatic clearance of insulin , resulting in dyslipoproteinemia, glucose intolerance, and hyperisulinemia. Lönnqvist et al.

They observed that males had a higher fat cell volume with no sex differences in the lipolytic sensitivity to β l - and β 2 -adrenoreceptor-specific agonists or in the antilipolytic effect of insulin. However, the lipolytic β 3 -adrenoreceptor sensitivity was 12 times higher in men, and the antilipolytic α2-adrenoreceptor sensitivity was 17 times lower in men.

It was concluded that in obesity, the catecholamine-induced rate of FFA mobilization from visceral fat to the portal venous system is higher in men than women. This phenomenon is partly due to a larger fat cell volume, a decrease in the function ofα 2-adrenoceptors, and an increase in the function of β 3 -adrenoreceptors.

These factors may contribute to gender-specific differences observed in the metabolic disturbances accompanied by obesity, i. Glucocorticoid receptors. Glucocorticoid receptors, one of the most important receptors for human adipose tissue function, are involved in metabolic regulation and distribution of body fat under normal as well as pathophysiological conditions.

Glucocorticoid receptors in adipose tissue show a regional variation in density with elevated concentrations in visceral adipose tissue In spite of the lower receptor density, the elevated cortisol secretion results in clearly increased net effects of cortisol.

Androgen and estrogen receptors. Adipocytes have specific receptors for androgens, with a higher density in visceral fat cells than in adipocytes isolated from subcutaneous fat. Unlike most hormones, testosterone induces an increase in the number of androgen receptors after exposure to fat cells , thereby affecting lipid mobilization.

This is more apparent in visceral fat omental, mesenteric, and retroperitoneal because of higher density of adipocytes and androgen receptors, in addition to other factors However, at variance with the effects of testosterone, dihydrotestosterone treatment does not influence lipid mobilization In females, there is an association between visceral fat accumulation and hyperandrogenicity, despite the documented effects of testosterone on lipid mobilization and the expected decrease in visceral fat depots.

The observation that visceral fat accumulation occurs only in female-to-male transsexuals after oophorectomy suggests that the remaining estrogen production before oophorectomy was protective The androgen receptor in female adipose tissue seems to have the same characteristics as that found in male adipose tissue.

However, estrogen treatment down-regulates the density of this receptor, which might be a mechanism whereby estrogen protects adipose tissue from androgen effects. Estrogen by itself seems to protect postmenopausal women receiving replacement therapy from visceral fat accumulation Estrogen receptors are expressed in human adipose tissue and show a regional variation of density, but whether the quantity of these receptors is of physiological importance has not been clearly established With regard to progesterone, adipose cells seem to lack binding sites and mRNA for progesterone receptors, indicating that progesterone acts through glucocorticoid receptors GH receptors.

While it is well established that GH has specific and receptor-mediated effects in adipose tissue of experimental animals, the importance of GH receptors in human adipose tissue is not fully elucidated at present although the available data indicate a functional role.

However, GH is clearly involved in the regulation of visceral fat mass in humans. Acromegaly, a state of GH excess, is associated with decreased visceral fat while in GH deficiency there is an increase in visceral fat and in adults with GH deficiency, recombinant human GH replacement therapy results in adipose tissue redistribution from visceral to subcutaneous locations; however, the regulation of adipose tissue metabolism requires synergism with steroid hormones A direct demonstration of a regulation of the GH receptor in human fat cells has not yet been performed Thyroid hormone receptors.

Thyroid hormones have multiple catabolic effects on fat cells as a result of interactions with the adrenergic receptor signal transduction system, and most of these interactions are also present in human fat cells There are data regarding the characterization of the nuclear T 3 receptor in human fat cells Although receptor regulation has not yet been demonstrated, there is little doubt that the thyroid hormone receptors are important for the function of human adipose tissue Further, no data are available on the correlation between visceral fat mass and thyroid hormone levels.

Adenosine receptors. Adenosine behaves as a potent antilipolytic and vasodilator agent and can be considered as an autocrine regulator of both lipolysis and insulin sensitivity in human adipose tissue. Site differences in ambient adenosine concentration, perhaps controlled by blood flow, may also modulate adipose tissue metabolism 7.

Adenosine content is higher in omental than in abdominal subcutaneous adipose tissue, but the receptor-dependent inhibition of lipolysis is, as indicated before , less pronounced in the former than in the latter depot However, despite strong antilipolytic effect of adenosine analogs, human adipocytes contain few adenosine type A l receptors, regardless of the fat depot considered According to Arner , the α2-, β l -,β 2 -, and β 3 -adrenoreceptors and receptors for insulin, adenosine, and glucocorticoids, as well as for PGE 2 , a potent antilipolytic agent with high affinity receptors identified in adipocytes , have a major functional role, as shown by relevant biological receptor-mediated effects, the presence of a receptor molecule, and receptor regulation.

The receptors for GH, thyroid hormones, estrogen, and testosterone, as well as for acetylcholine and TSH, probably have an important functional role but complete evidence, indicated in the previous group of receptors, is not present so far; however, there is little doubt of a regulatory role.

Genetic epidemiology: heritability and segregation analysis. Studies performed in individuals from families of French descent living in Quebec City [Quebec Family Study QFS ] allowed the estimation of the fraction of the phenotypic variance that could be attributed to the genetic and environmental factors among the obesity phenotypes or in the distribution of the adipose tissue, taking into account the BMI and amount of subcutaneous fat by the sum of the measurement of skinfolds in six different sites , lean body mass, fat mass, percentage of fat derived from underwater weighing, and visceral fat by CT , The residual variance corresponded to environmental factors, but some factors cultural, nongenetic could be transmitted from parents to descendents and sometimes were confounded by genetic effects Segregation analysis studies have recently concluded that visceral fat is similarly influenced by a gene with a major effect in the QFS and HERITAGE families , However, after adjustment of the visceral adipose tissue for the fat mass, the effect of the gene with the major effect was not more compatible with a mendelian transmission.

These results suggested the presence of a pleiotropism: the gene with the major effect, identified by the fat mass , could similarly influence the amount of visceral fat Similar results were obtained with the same type of analysis in the HERITAGE cohort To test the hypothesis of a genetic pleiotropism, Rice et al.

The results of this study Fig. These results have confirmed the presence of a genetic pleiomorphism and suggested the presence of genes affecting simultaneously the amounts of fat mass and visceral abdominal fat. Schematic representation of the genetic effects on total fat mass and visceral fat adjusted for the fat mass and on the co-variation between the two phenotypes Quebec Family Study, G 1 and G 2 represent the genetic effects specific for the total fat mass and visceral fat, respectively.

E 1 and E 2 represent the specific effects of the environment on total fat mass and visceral fat, respectively. G 3 and E 3 indicate the genetic and environment effects common to both phenotypes.

Pérusse et al. The interactions of the effects of genotype and environment evaluated in monozygotic twins, when the energy balance is manipulated, indicated that even though there were large interindividual differences in the response to excess or negative energy balance, there was a significant within-pair resemblance in response 96 , In effect, in response to overfeeding, there was at least 3 times more variance in response between pairs than within pairs for the gains in body weight, fat mass, and fat-free mass In relation to the response to the negative energetic balance, at least 7 times more variation was observed in response between pairs than within members of the same pair of twins, with respect to the same variables This intrapair similarity in the response to either excess or deficient energy balance is also observed in relation to the abdominal visceral fat Thus, the interaction between genotype and environment is important to consider in the study of the genetics of obesity since the propensity to fat accumulation is influenced by the genetic characteristics of the subject.

Molecular genetics: association and linkage studies. Several candidate genes as well as random genetic markers were found to be associated with obesity as well as body fat and fat distribution in humans. The current human obesity gene map, based on results from animal and human studies, indicates that all chromosomes, with the exception of the Y chromosome, include genes or loci potentially involved in the etiology of obesity Initial findings from the QFS showed that significant but marginal associations with body fat were found with LPL and the α2-subunit of the sodium-potassium ATPase genes The Trp64Arg mutation of the β 3 -adrenergic receptor gene β 3 AR , prevalent in some ethnic groups, is associated with visceral obesity and insulin resistance in Finns as well as increased capacity to gain weight This mutation was also shown to be associated with abdominal visceral obesity in Japanese subjects, with lower triglycerides in the Trp64Arg homozygotes but not heterozygotes It has been suggested that those with the mutation may describe a subset of subjects characterized by decreased lipolysis in visceral adipose tissue.

On the other hand, Vohl et al. Previously, it was reported by the same group that apo-B gene Eco R-1 polymorphism appeared to modulate the magnitude of the dyslipidemia generally found in the insulin-resistant state linked with visceral obesity These studies are a demonstration of a significant interaction between visceral obesity and a polymorphism for a gene playing an important role in lipoprotein metabolism.

When the genes related to the hormonal regulation of body fat distribution studied in the QFS families sex hormone-binding globulin, 3β-hydroxysteroid dehydrogenase, and glucocorticoid receptor genes were considered along with the knowledge that body fat distribution is influenced by nonpathological variations in the responsiveness to cortisol, it was shown that the less frequent 4.

However, the association with abdominal visceral fat area was seen only in subjects of the lower tertile of the percent body fat level.

The consistent association between the glucocorticoid receptor polymorphism detected with Bcl I and abdominal visceral fat area suggested that this gene or a locus in linkage disequilibrium with the Bcl I restriction site may contribute to the accumulation of abdominal visceral adipose tissue With respect to the linkage studies, only a few studies of body fat or fat distribution with random genetic markers or candidate genes have been reported using the sibling-pair linkage method.

One of the few reported studies relative to the visceral fat mass was the evaluation of a sib-pair linkage analysis from the QFS between five microsatellite markers encompassing about 20 cM in the Mob-1 region of the human chromosome 16pp These results suggested to the authors that this region of the human genome contains a locus affecting the amount of visceral fat and lipid metabolism as also shown by the association studies indicated above.

The other population and intrafamily association study used a polymorphic marker LIPE in the hormone-sensitive lipase gene, located on chromosome 19q In conclusion, despite the fact that the genetic architecture of obesity has just begun, the results obtained so far suggest that a great number of genes, loci, or chromosomal regions distributed on different chromosomes could play a role in determining body fat and fat distribution in humans.

This reflects the complex and heterogeneous nature of obesity. The accumulation of adipose tissue in the abdominal region is at least partially influenced by genes, which becomes more evident as the number of involved genes are identified.

The concept that adipocytes are secretory cells has emerged over the past few years. Adipocytes synthesize and release a variety of peptide and nonpeptide compounds; they also express other factors, in addition to their ability to store and mobilize triglycerides, retinoids, and cholesterol.

These properties allow a cross-talk of adipose tissue with other organs as well as within the adipose tissue. The important finding that adipocytes secrete leptin as the product of the ob gene has established adipose tissue as an endocrine organ that communicates with the central nervous system.

As already mentioned, LPL is the key regulator of fat cell triglyceride deposition from circulating triglycerides. LPL is found, after transcytosis, associated with the glycosaminoglycans present in the luminal surface of the endothelial cells.

The regulation of LPL secretion, stimulated by the most important hormonal regulator, insulin, is related to posttranslational changes in the LPL enzyme, at the level of the Golgi cisternae and exocytotic vesicles, insulin possibly having a positive role in this secretory process Genes encoding LPL were not differentially expressed in omental when compared with subcutaneous adipocytes However, in very obese individuals omental adipocytes express lower levels of LPL protein and mRNA than do subcutaneous fat cells The regulation of LPL in obesity has been presented in the Section on correlations of abdominal visceral fat.

With respect to the hormonal regulation of LPL, insulin and glucocorticoids are the physiological stimulators of the LPL activity, and their association plays an important role in the regulation of body fat topography.

In effect, omental adipose tissue is known to be less sensitive to insulin, both in the suppression of lipolysis and in the stimulation of LPL However, when exposed to the combination of insulin plus dexamethasone in culture for 7 days, large increases in adipose LPL were observed because of increases in LPL mRNA Significant differences were observed between men and women.

The increase in LPL in response to dexamethasone suggests that the well known steroid-induced adipose redistribution especially in the abdomen may be caused by increases in LPL, which would lead to a preferential distribution of plasma triglyceride fatty acids to the abdominal depot.

Therefore, these data suggest that LPL is central to the development of abdominal visceral obesity On the other hand, catecholamines, GH, and testosterone in males reduce adipose tissue LPL Acylation-stimulating protein ASP.

ASP is considered the most potent stimulant of triglyceride synthesis in human adipocytes yet described. Its generation is as follows Human adipocytes secrete three proteins of the alternate complement pathway: C3 the third component of the complement , factor B, and factor D adipsin , which interact extracellularly to produce a amino-terminal fragment of C3 known as C3a.

Excess carboxypeptidases in plasma rapidly cleave the terminal arginine from C3a to produce the amino acid peptide known as C3a desarg or ASP, which then acts back upon the adipocyte, causing triglyceride synthesis to increase. As fatty acids are being liberated from triglyceride-rich lipoproteins and chylomicrons as the result of the action of LPL, ASP is also being generated and triglyceride synthesis increased concurrent with the need to do so.

In human adipose tissue, in the postprandial period, ASP secretion and circulating triglycerides clearance are coordinated in accordance with the suggestion that ASP in sequence to LPL would have a paracrine autoregulatory role.

The adipsin-ASP pathway, therefore, links events within the capillary space to the necessary metabolic response in the subendothelial space, thus avoiding the excess buildup of fatty acids in the capillary lumen.

The generation of ASP is triggered by chylomicrons. While insulin decreases gene expression of C3, B, and adipsin, it enhances the secretion of ASP as expected from the concurrent action of LPL and ASP. However, more intensely and independent of insulin, ASP is capable of stimulating triglyceride synthesis in adipocytes and fibroblasts.

Thus, from the reduced sensitivity to insulin in the suppression of lipolysis and stimulation of LPL by the omental adipose tissue, omental obesity may represent an example of impaired activity of the ASP pathway even if dysfunction of the pathway is a secondary feature.

As a consequence, omental adipose tissue, as compared with subcutaneous fat tissue, would have a limited capacity to prevent fatty acids from reaching the liver, which may contribute to the abnormalities in metabolism observed in visceral obesity Cholesteryl-ester transfer protein CETP.

Human adipose tissue is rich in CETP mRNA, probably one of the major sources of circulating CETP in humans. CETP promotes the exchange of cholesterol esters of triglycerides between plasma lipoproteins.

In this way, the adipose tissue is a cholesterol storage organ in humans and animals; peripheral cholesterol is taken up by HDL species, which act as cholesterol efflux acceptors, and is returned to the liver for excretion , The few studies of circulating CETP in obesity have shown that activity and protein mass of CETP are both significantly increased in obesity, being negatively correlated with HDL cholesterol and the cholesteryl ester-triglyceride ratio of HDL2 and HDL3, thus exhibiting an atherogenic lipoprotein profile.

Furthermore, there was a positive correlation with fasting plasma insulin and blood glucose, suggesting a possible link to insulin resistance — From an observation of Angel and Shen , it could be suggested that the CETP activity of omental adipose tissue is greatly increased in comparison with subcutaneous fat.

Retinol-binding protein RBP. Adipose tissue is importantly involved in retinoid storage and metabolism. RBP is synthesized and secreted by adipocytes , the rate of RBP gene transcription being induced by retinoic acid The mRNA encoding RBP is expressed at a relatively high level in adipocytes with no difference between subcutaneous and omental fat cells There are no data regarding retinol mobilization from adipose stores in humans; however, in vitro studies with murine adipocytes showed that the cAMP-stimulated retinol efflux from fat cells was not the result of increased RBP secretion but instead due to the hydrolysis of retinyl esters by the cAMP-dependent hormone-sensitive lipase PAI-1 is a serine protease inhibitor and evidence suggests that it is a major regulator of the fibrinolytic system, the natural defense against thrombosis.

It binds and rapidly inhibits both single- and two-chain tissue plasminogen activator tPA and urokinase plasminogen activator uTPA , which modulate endogenous fibrinolysis. The major sources of PAI-1 synthesis are hepatocytes and endothelial cells, but platelets, smooth muscle cells, and adipocytes are also contributors The increased gene expression and secretion of PAI-1 by adipose tissue contribute to its elevated plasma levels in obesity, presenting a strong correlation with parameters that define the insulin resistance syndrome, in particular with fasting plasma insulin and triglycerides, BMI, and visceral fat accumulation: omental adipose tissue explants produced significantly more PAI-1 antigen than did subcutaneous tissue from the same individual, and transforming growth factor-βl increased PAI-1 antigen production In a premenopausal population of healthy women with a wide range of BMI, there was a positive correlation of PAI-1 activity with CT-measured visceral fat area, independent of insulin and triglyceride levels.

Weight loss confirmed this link. PAI-1 diminution was correlated only with visceral adipose tissue area loss and not with total fat, insulin, or triglyceride decrease Losing belly fat is a common goal.

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Medical News Today. Health Conditions Health Products Discover Tools Connect. Ways to lose subcutaneous fat. Medically reviewed by Daniel Bubnis, M. Causes Difficulty to lose Strategies to shed Connection to health Subcutaneous fat is fat that is visible just under the skin. What causes it and why is it hard to lose?

Why is it so hard to lose? Strategies for shedding subcutaneous fat. Subcutaneous fat and health. How we reviewed this article: Sources. Medical News Today has strict sourcing guidelines and draws only from peer-reviewed studies, academic research institutions, and medical journals and associations.

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How gastric bypass surgery can help with type 2 diabetes remission. Molecular and cellular biology 35 , — Esteve Rafols, M. Adipose tissue: cell heterogeneity and functional diversity. Endocrinologia y nutricion: organo de la Sociedad Espanola de Endocrinologia y Nutricion 61 , — Article Google Scholar.

Macotela, Y. Intrinsic differences in adipocyte precursor cells from different white fat depots. Diabetes 61 , — Sanchez-Gurmaches, J. Adipocytes arise from multiple lineages that are heterogeneously and dynamically distributed.

Nature communications 5 , Download references. holds the Dr. Charles A. Allard Chair in Diabetes Research. This research was supported by operating grants to P. Rod Eidem Diabetes Research Fund. and P. Student funding was provided by the Alberta Diabetes Foundation K.

received post-doctoral funding from the Juvenille Diabetes Research Foundation. received funding from an American Diabetes Association Jr. Faculty Award JDF is a postdoctoral FWO [PEGASUS] Marie Skłodowska-Curie Fellow.

Alberta Diabetes Institute, Department of Pharmacology, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, T6G 2E1, Canada.

Division of Plastic Surgery, Department of Surgery, Faculty of Medicine and Dentistry, University of Alberta, Edmonton Alberta, T6G 2B7, Canada.

Department of Biochemistry, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, T6G 2E1, Canada. Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, OH, , USA.

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Abstract Subcutaneous white adipose tissue scWAT is the major fat depot in humans and is a central player in regulating whole body metabolism.

Introduction Dysfunctional white adipose tissue WAT is associated with the development of obesity, diabetes and cardiovascular disease 1. Results scWAT adipocytes possess physiologically relevant blue light-sensitive inward currents As bright white light is typically used in electrophysiology and many bi-stable opsins can inactivate under broad-spectrum light 21 , 22 , adipocytes were kept under red light to visualize the positioning of the recording pipette Fig.

Figure 1. Full size image. Figure 2. Figure 3. Figure 4. Methods Experimental models Human scWAT Tissue samples were obtained from subjects undergoing abdominoplasty surgery in accordance with institutional human ethics guidelines and informed consent was obtained from all subjects.

Mouse scWAT All animal study protocols for tissue isolation were approved by University of Alberta Animal Care and Use Committee protocol s AU and AU SGBS adipocytes The Simpson-Golabi-Behmel Syndrome SGBS human pre-adipocyte cell strain was provided by Dr. Method details Electrophysiology The whole-cell patch-clamp technique was used to record currents from differentiated adipocytes.

Reverse transcriptase PCR Total RNA was isolated from all samples using TRIzol Reagent ThermoFisher Scientific, Waltham, MA, USA and then reverse transcribed using qScript cDNA SuperMix, Quanta Biosciences, Beverly, MA, USA.

Table 1 Primer sets used for the PCR and nested PCR experiments detailed in Fig. Full size table. References Hevener, A. Article CAS Google Scholar Lee, M. Article CAS PubMed Google Scholar Misra, A.

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Acknowledgements P. Lee Authors Katarina Ondrusova View author publications. View author publications. Ethics declarations Competing Interests The authors declare that they have no competing interests.

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Rights and permissions Open Access This article is licensed under a Creative Commons Attribution 4. About this article. Cite this article Ondrusova, K. Copy to clipboard. This article is cited by Melanopsin-mediated optical entrainment regulates circadian rhythms in vertebrates Deng Pan Zixu Wang Jing Cao Communications Biology Sensing of Physical Factors by Cells: Electric Field, Mechanical Forces, Physical Plasma and Light—Importance for Tissue Regeneration Meike Bielfeldt Henrike Rebl J.

Giebultowicz npj Aging Metabolic responses of light and taste receptors — unexpected actions of GPCRs in adipocytes Onyinye Nuella Ekechukwu Mark Christian Reviews in Endocrine and Metabolic Disorders Significance and Application of Light Therapy Based on Photoreceptors to the Regulation of Fat Metabolism Mari Sato Current Oral Health Reports Comments By submitting a comment you agree to abide by our Terms and Community Guidelines.

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What Is Subcutaneous Fat? February Author information Authors and Affiliations Department of Medicine H7 , Karolinska Institutet at Karolinska University Hospital Huddinge, Center for Metabolism and Endocrinology, , Stockholm, Sweden Peter Arner, Daniel P. Furthermore, leptin expression and levels increase as the size of the adipose tissue triglyceride stores increase Series A, Biological Sciences and Medical Sciences. Close Search. Although, this would decrease the number of comparable EOO and LOO subjects considerably and lower the statistical power. READ MORE.
Taking aim at belly fat Effects of age, gender, BMI, and anatomical site on skin thickness in children and adults with diabetes. Dynamics of fat cell turnover in humans. d — f Is lipolysis expressed per number of fat cells. Evidence for a major role of skeletal muscle lipolysis in the regulation of lipid oxidation during caloric restriction in vivo. Oil Red-O lipid ORO staining was used to assess changes in lipid homeostasis on day 14 of the chronic light stimulation protocol after the last day of light exposure day
Subcutaneous fat is Eco-friendly products online that is cdlls just under Subcutanneous skin. Ways of Subcutaneous fat cells Herbal digestion aids include swapping some carbohydrates for uSbcutaneous, doing aerobic exercise, and managing mental health issues. Subcutaneous fat is normally harmless and may even protect against some diseases. Visceral fat is fat that surrounds the organs. Though it is not visible from the outside, it is associated with numerous diseases. It is possible to lose both subcutaneous and visceral fat.

Subcutaneous fat cells -

According to Abate et al. However, the lack of exact borderlines between these two depots on CT or MRI makes this subdivision only an approximation. Even a large error in the delineation between these two tissues would lead to the conclusion that, at least in men, the retroperitoneal fat mass is a minor part of intraabdominal adipose mass, comprising only approximately one fourth of visceral fat Abate et al.

Märin et al. Similarly, Abate et al. Thus, their investigation, as well as that of Goodpaster et al. The WHR is the most widely used index of regional adipose tissue distribution and is measured in a standing position.

Waist circumference is defined as the minimal circumference measured at the navel, and the hip circumference is defined as the widest circumference measured at the hips and buttocks There is a well documented sex dimorphism in regional adipose tissue distribution Indeed, despite the fact that women are usually more obese as a group than men, male subjects more frequently have significantly higher mean waist circumference and higher mean WHR in agreement with the greater propensity of men to accumulate excess fat within the abdominal cavity.

Thus, the threshold values suggested by Pouliot et al. Thus it was effective in predicting aberrations in glucose and insulin levels and also showed a strong correlation between plasma lipids and blood pressure WHR predicted subsequent diabetes in men 13 and coronary heart disease in both men and women 8 , 9 and was more predictive of these endpoints than either the BMI or a more complex procedure using the sum of multiple skinfold thicknesses.

Its effects are independent of the overall level of obesity. However, Pouliot et al. Thus, according to their data, the WHR determines the regional distribution of adipose tissue, which is relatively independent of the degree of obesity and appears less closely related to the amount of abdominal visceral adipose tissue.

In this study 38 , other simple anthropometric indexes were evaluated that appeared to be superior to the WHR in providing assessment of visceral obesity, waist circumference, and abdominal sagittal diameter to be discussed below. Similar conclusions were reached by Sjöström et al.

Waist circumference. For example, the waist circumference is correctly measured at the level of the umbilicus, but in many obese individuals, the umbilicus may be directed downward because of the excessive curvatures of the abdominal wall. Waist circumference measured at the midpoint between the lower border of the rib cage and the iliac crest has been reported to be more closely correlated with the level of abdominal visceral adipose tissue and associated metabolic variables than the WHR in both sexes 38 , 42 , 44 , According to Pouliot et al.

The threshold value is similar in men and women in that for a given waist circumference, men and women had comparable levels of abdominal visceral adipose tissue. Thus, waist circumference, a convenient and simple measurement unrelated to height 46 and correlated with BMI and WHR 47 , determines the extension of abdominal obesity, which appears closely linked to abdominal visceral adipose tissue deposition.

Furthermore, while changes in waist girth reflect changes in risk factors for cardiovascular disease 48 and other forms of chronic disease, the risks vary in different populations; therefore, globally applicable cut-off points cannot be developed.

For example, abdominal fatness has been shown to be less strongly associated with risk factors for cardiovascular disease and type 2 diabetes in black women than in white women Risk factors such as total and HDL cholesterol were correlated with subcutaneous and abdominal fat areas by CT as well as their sum in healthy nonobese Asian Indians.

On the other hand, while there was an association of visceral adiposity with insulin secretion during an oral glucose test in men, such was not found in women In addition, it has been reported that visceral obesity is strongly related to coronary heart disease risk factors in nonobese Japanese-American men Also, people of South Asian Indian, Pakistani, and Bangladeshi descent living in urban societies have a higher incidence of obesity complications than other ethnic groups These complications are seen to be associated with abdominal fat distribution, which is markedly higher for a given level of BMI than in Europeans.

Finally, although women have an almost equivalent absolute risk of coronary heart disease CHD to men at the same WHR 53 , 54 , they show increases in relative risk of CHD at lower waist circumferences than men. Thus, there is a need to develop sex-specific waist circumference cut-off points appropriate for different populations.

The studies by Ferland et al. Therefore, the waist circumference, and the abdominal sagittal diameter as will be discussed below , are the anthropometric indexes preferred over the WHR to estimate the amount of abdominal visceral fat and related cardiovascular risk profile.

Using the equations for prediction, multiscan CT was used to determined visceral adipose tissue volume from the waist circumference in a sample of 17 males and 10 females with different degrees of obesity Again, it was concluded that the WHR is a suboptimal predictor of visceral adipose tissue volume.

Abdominal sagittal diameter. The sagittal diameter is measured with a ruler as the vertical distance from the horizontal spirit level to the examination table after a normal expiration Kvist et al. The correlation of the sagittal diameter with visceral fat volume was 0. The correlations between the waist circumference and visceral fat were, respectively, 0.

These correlations are considerably higher than those observed between anthropometric variables and the visceral fat area measured at the level of the umbilicus in obese men and women Ferland et al.

Desprès et al. Busetto et al. It is very likely, therefore, that the range of fatness in subjects studied greatly influences the magnitude of the correlations and perhaps also the comparison between the sagittal diameter and the waist circumference with regard to their utility in predicting intraabdominal fat.

In addition, the distinction between studies that used only visceral fat area and those that calculated visceral fat volume from multiple scans may be important to make Ross et al.

A study from the Canadian group 38 conducted in a large group of males and females evaluated systematically the three anthropometric indexes and their association with abdominal visceral adipose and subcutaneous areas measured by CT between the fourth and fifth lumbar vertebrae and metabolic profile.

As seen in Table 1 , there was a strong association between waist girth and body fat mass, the slope of the regression line being steeper in women data not shown. With relation to the abdominal visceral fat area, for a given waist circumference, men and women had similar levels and the slopes of the regression lines were not different between genders.

Essentially similar results were observed with the abdominal sagittal diameter. However, in contrast with waist circumference, the slopes of regression of abdominal sagittal diameter to abdominal visceral fat area were significantly different between genders and were steeper in men data not shown.

Finally, it can be seen that the WHR was less strongly correlated with total body fat mass and abdominal visceral and subcutaneous areas than the other indexes. This study demonstrated that most of the variance in waist girth and abdominal sagittal diameter can be explained by variations in body fat mass and in abdominal visceral and subcutaneous adipose tissue areas 0.

With relation to the metabolic variables related to cardiovascular risk plasma triglycerides and high-density lipoprotein cholesterol levels, fasting and postglucose glucose and insulin levels , in women, the waist circumference and the abdominal sagittal diameter were more closely related to the metabolic variables than the WHR, whereas such differences were not apparent in men.

They concluded that waist circumference values above approximately cm, abdominal sagittal diameter values greater than 25 cm, and WHR values greater than 0. Correlations r values between the anthropometric indexes and body fat mass, abdominal visceral, and abdominal subcutaneous fat areas in 81 men and 70 women.

Correlations between sagittal diameter and waist circumference are usually quite high [ e. Although the sagittal supine diameter can be studied with relatively good precision 61 , it is clear that this measurement requires appropriate equipment and skilled personnel.

Since most people are measuring the WHR as an indicator of visceral fat, the focus should be switched to the waist girth alone without affecting the ranking of individuals with respect to visceral fat when based on the waist circumference compared with the sagittal diameter Computed tomography CT.

CT can be considered the gold standard not only for adipose tissue evaluation but also for multicompartment body measurement 61 , The reported error for the determination of total adipose tissue volume after performing 28 scans is 0.

The subcompartments of adipose tissue volume, visceral and subcutaneous adipose tissue, can be accurately measured with errors of 1. In eight nonobese Swedish males evaluated by the multiscan CT technique, the volume of visceral abdominal adipose tissue in the intraperitoneal and retroperitoneal compartments was found to be 1.

Using a multislice magnetic resonance protocol, Abate et al. In effect, in 13 lean males, Abate et al. If only one scan is used to measure the visceral adipose tissue area, a strictly defined longitudinal level is very important since the average visceral adipose tissue area shifts if there is a change in position, even of a few centimeters.

This, according to Sjöström et al. Instead, the longitudinal level must be defined in a strict relation to the skeleton, usually between the L4 and L5 vertebrae.

The subjects are examined in a supine position with their arms stretched above their heads. The choice to perform the scan at the level of the umbilicus was initially proposed by Borkan et al.

Subsequently, Tokunaga et al. In addition to the recommendations of the Japanese investigators, studies from Korea 20 and from our clinic use the scan at the umbilicus.

Visceral fat is defined as intraabdominal fat bound by parietal peritoneum or transversalis fascia, excluding the vertebral column and the paraspinal muscles; subcutaneous fat is fat superficial to the abdominal and back muscles.

Subcutaneous fat area is calculated by subtracting the intraabdominal fat area from the total fat area. In addition, visceral fat increases with age Figure 1 shows cross-sectional abdominal areas obtained by CT at the level of the umbilicus in two women matched for the same BMI, who differed markedly in the accumulation of fat in the abdominal cavity but less so in the subcutaneous abdominal fat.

Computed tomography showing cross-sectional abdominal areas at umbilicus level in two patients demonstrating variation in fat distribution. A, Visceral type yr-old female, B, Subcutaneous type yr-old female, In obese subjects the level of the umbilicus can change from one patient to another, thus changing the visceral adipose tissue area; therefore, it is advisable that the scan area be defined in strict relation to the skeleton.

Chowdhury et al. However, the values for abdominal cut-off points were related to increased cardiovascular risk Table 2. Using the scan at the umbilicus as described by several investigators gave results similar to, although somewhat lower than, those reported using the L4-L5 level. Abdominal visceral adipose tissue area cut-off points related to increased cardiovascular risk.

Regarding the relationship between the modifications in subcutaneous and visceral adipose tissue, with changes in body weight, it was shown that after severe weight loss, subcutaneous fat at the abdominal level is lost in greater proportion than visceral fat, but the mechanism of these differential changes in both compartments of abdominal fat is unknown, suggesting that visceral fat does not reflect nutritional status to the extent that sc fat does In the same way, published data suggest that, at least in relative terms, visceral fat increases less than subcutaneous fat with increased body weight However, because the amount of subcutaneous abdominal fat is calculated indirectly, it is likely that significant measurement error could be introduced Regarding the reproducibility of CT measurement of visceral adipose tissue area, Thaete et al.

The duplication occurred after the initial scan; the subjects were repositioned before repeat scanning. As indicated in the Introduction , individuals with a high accumulation of visceral abdominal fat, as shown by CT scans, had an increased risk for development of type 2 diabetes, dyslipidemia, and coronary heart disease.

Table 2 shows the thresholds above which metabolic complications would be more likely to be observed in visceral adipose tissue areas. Desprès and Lamarche 73 , Hunter et al.

They found that a value above cm 2 was associated with an increased risk of coronary heart disease in pre and postmenopausal women 75 ; the same group 74 found that males with abdominal visceral fat cross-section areas measuring more than cm 2 were clearly at an increased risk for coronary disease.

On the other hand, Desprès and Lamarche 73 found that in both men and women a value of cm 2 was associated with significant alterations in cardiovascular disease risk profile and that a further deterioration of the metabolic profile was observed when values greater than cm 2 of visceral adipose tissue were reached.

From the same center, Lemieux et al. It was concluded that waist circumference was a more convenient anthropometric correlate to visceral adipose tissue because its threshold values did not appear to be influenced by sex or by the degree of obesity.

Anderson et al. The most extensive studies using a single CT scan at umbilical level was done by Matsuzawa and colleagues 17 , However, they did not present the raw data on visceral and subcutaneous areas but only their ratios, thus precluding their inclusion in Table 2. In another study, performed in Japan by Saito et al.

Lottenberg et al. Magnetic resonance imaging MRI. MRI provided results similar to CT without exposure to ionizing radiation, the main problem with CT multislice measurements.

It demonstrated good reproducibility for total and visceral adipose tissue volumes 63 , which were slightly lower than previously reported using CT 55 , although the percent contribution of visceral to total adipose tissue volume was similar 18 vs.

Subcutaneous adipose tissue and visceral fat areas at the L4-L5 level determined in 27 healthy men by MRI were These areas were highly predictive of the corresponding volume measurements computed from the scan MRI, confirming the CT studies of Kvist et al.

Two studies have compared estimates of subcutaneous and visceral adipose tissue by CT and MRI. Comparison between MRI and CT in seven subjects showed a high degree of agreement in measurement of total subcutaneous adipose tissue area but not visceral adipose tissue area As already mentioned, MRI has been validated in three cadavers, confirming its accuracy Ultrasound US.

US subcutaneous and intraabdominal thicknesses, the latter corresponding to the distance between abdominal muscle and aorta, were measured 5 cm from the umbilicus on the xipho-umbilical line with a 7. The intraindividual reproducibility of US measurements was very high both for intraabdominal and subcutaneous thickness as well as for interoperators 83 , Several studies demonstrated a highly significant correlation between the intraabdominal adipose tissue determined by CT and by US.

A decade ago, Armellini et al. In a more recent study, Tornaghi et al. In a study of men C. Leite, D. Matsuda, B. Wajchenberg, G. Cerri, and A. Halpern, unpublished data , in which In obese women, after a 6-kg weight loss, a significant decrease was found in intraabdominal fat but not in subcutaneous adipose tissue, as determined by both CT and US There was also a significant correlation between changes in intraabdominal adipose tissue using both techniques, indicating that US can be used in the evaluation of body fat distribution modifications during weight loss.

This is another confirmation of the reliability of the US intraabdominal determinations. The amount of visceral fat increases with age in both genders, and this increase is present in normal weight BMI, In a study of subjects 62 males and 68 females with a wide range of age and weight , Enzi et al.

This fat topography was retained in young and middle-aged females up to about 60 yr of age, at which point there was a change to an android type of fat distribution. This age-related redistribution of fat is due to an absolute as well as relative increment in visceral fat depots, particularly in obese women, which could be related to an increase in androgenic activity in postmenopausal subjects.

On the other hand, they showed that males at any age tend to accumulate fat at the visceral depot, increasing with age and BMI increase. In the male, a close linear correlation between age and visceral fat volume was shown, suggesting that visceral fat increased continuously with age Although this correlation was also present in women, the slope was very gentle in the premenopausal condition.

It became steeper in postmenopausal subjects, almost the same as in males Further, Enzi et al. From the published data 68 , 90 , it can be concluded that both subcutaneous and visceral abdominal fat increase with increasing weight in both sexes but while abdominal subcutaneous adipose tissue decreases after the age of 50 yr in obese men, it increases in women up to the age of 60—70 yr, at which point it starts to decline Fowler et al.

Finally, as previously indicated, visceral fat is more sensitive to weight reduction than subcutaneous adipose tissue because omental and mesenteric adipocytes, the major components of visceral abdominal fat, have been shown to be more metabolically active and sensitive to lipolysis Lemieux et al.

In addition, the adjustment for differences in visceral fat between men and women eliminated most of the sex differences in cardiovascular risk factors.

There is evidence supporting the notion that abdominal visceral fat accumulation is an important correlate of the features of the insulin-resistant syndrome 23 , 24 , 29 but this should not be interpreted as supporting the notion of a cause and effect relationship between these variables This subject will be discussed later on.

The correlations of abdominal visceral fat mass evaluated by CT or MRI scans with total body fat range from 0. They tend to be lower in the lean and normal weight subjects than in the obese As indicated by Bouchard et al.

When they examined the relationship of total body fat mass to visceral adipose tissue accumulation in men and in premenopausal women, Lemieux et al. Furthermore, the relationship of visceral adipose tissue to metabolic complications was found to be independent of concomitant variation in total body fat, and it was concluded that the assessment of cardiovascular risk in obese patients solely from the measurement of body weight or of total body fatness may be completely misleading 19 , 22 , 36 , Indeed, it appears that only the subgroup of obese individuals characterized by a high accumulation of visceral adipose fat show the complications predictive of type 2 diabetes and cardiovascular disease On the other hand, after adjustment for total body fat, Abate et al.

Intraabdominal visceral fat is associated with an increase in energy intake but this is not an absolute requirement.

Positive energy balance is a strong determinant of truncal-abdominal fat as shown by Bouchard and colleagues 96 in overfeeding experiments in identical twins.

The correlations between gains in body weight or total fat mass with those in subcutaneous fat on the trunk reached about 0. In contrast, these correlations attained only 0. Thus, positive energy balance does not appear to be a strong determinant of abdominal visceral fat as is the case with other body fat phenotypes 7.

In effect, as discussed in the CT section of imaging techniques for evaluation of intraabdominal visceral fat, some investigators 70 , 71 have shown that either when the subjects lose or increase their weight, particularly females, visceral fat is lost or gained, respectively, less than subcutaneous fat at the abdominal level.

However, at variance from these data, Zamboni et al. Similarly, as already mentioned, Smith and Zachwieja 32 noted that all forms of weight loss affect visceral fat more than subcutaneous fat percentage wise , and there was a gender difference, with men appearing to lose more visceral fat than women for any given weight loss.

LPL activity, being related to the liberation of the lipolytic products [from chylomicra and very-low-density lipoproteins VLDL ] to the adipocytes for deposit as triglycerides, is a key regulator of fat accumulation in various adipose areas, since human adipose tissue derives most of its lipid for storage from circulating triglycerides.

However, adipocytes can synthesize lipid de novo if the need arises, as in patients with LPL deficiency According to Sniderman et al.

The increase of visceral fat masses with increasing total body fat was explained by an increase of fat cell size only up to a certain adipocyte weight. However, with further enlargement of intraabdominal fat masses with severe obesity, the number of adipocytes seems to be elevated , In women, but not in men, omental adipose tissue has smaller adipocytes and lower LPL activity than subcutaneous fat depots since variations in LPL activity parallel differences in fat cell size 7.

When adipocytes enlarge in relation to a gain in body weight, the activity of LPL increases in parallel, possibly as a consequence of obesity-related hyperinsulinism.

The higher basal activity of adipose tissue LPL in obesity is accompanied by a lower increment after acute hyperinsulinemia Lipid accumulation is favored in the femoral region of premenopausal women in comparison with men In the latter, LPL activity as well as the LPL mRNA levels were greater in the abdominal than in gluteal fat cells, while the opposite was observed in women, suggesting that regional variation of gene expression and posttranslational modification of LPL could potentially account for the differences between genders in fat distribution With progressive obesity, adipose tissue LPL is increased in the depots of fat in parallel with serum insulin.

However, when obese subjects lost weight and became less hyperinsulinemic, adipose LPL increased further and the patients who were most obese showed the largest increase in LPL, suggesting that very obese patients are most likely to have abnormal LPL regulation, independent of the influence of insulin.

In response to feeding, the increase in LPL is, as indicated, due to posttranslational changes in the LPL enzyme. However, the increased LPL after weight loss involved an increase in LPL mRNA levels, followed by parallel increases in LPL protein and activity Because the response to weight loss occurred via a different cellular mechanism, it is probably controlled by factors different from the day-to-day regulatory forces.

In addition, because the very obese patients demonstrated a larger increase in LPL with weight loss than the less obese patients, these data suggest a genetic regulation of LPL that is most operative in the very obese The role of sex steroids, glucocorticoids, and catecholamines in the regulation of adipose tissue LPL activity in various fat depots will be discussed in the section on hormonal regulation of abdominal visceral fat.

Lipid mobilization and the release of FFA and glycerol are modulated by the sympathetic nervous system. Catecholamines are the most potent regulators of lipolysis in human adipocytes through stimulatory β l - and β 2 -adrenoreceptors or inhibitoryα 2-adrenoreceptors A gene that codes for a third stimulatory β -adrenoreceptor, β 3 -adrenoreceptor, is functionally active principally in omental adipocytes but also present in mammary fat and subcutaneous fat in vivo In both genders and independently of the degree of obesity, femoral and gluteal fat cells exhibit a lower lipolytic response to catecholamines than subcutaneous abdominal adipocytes, the latter showing both increased β l - and β 2 -adrenoreceptor density and sensitivity and reduced α2-adrenoreceptor affinity and number Refs.

The increased sensitivity to catecholamine-induced lipolysis in omental fat in nonobese individuals is paralleled by an increase in the amount of β l - and β 2 -receptors, with normal receptor affinity and normal lipolytic action of agonists acting at postadrenoreceptor steps in the lipolytic cascade , ; this is associated with enhanced β 3 -adrenoreceptor sensitivity, which usually reflect changes in receptor number in comparison with subcutaneous adipocytes , Comparison of lipolysis, antilipolysis, and lipogenesis in omental and subcutaneous fat in nonobese and obese individuals.

Adipocytes from obese subjects generally show increased lipolytic responses to catecholamines, irrespective of the region from which they are obtained, and enhanced lipolysis in abdominal compared with gluteo-femoral fat 21 , The antilipolytic effect is also reduced in vitro in obesity, both in omental and subcutaneous adipocytes The typical features of visceral fat, e.

An increased β 3 -adrenoreceptor sensitivity to catecholamine stimulation may lead to an increased delivery of FFA into the portal venous system, with several possible effects on liver metabolism.

These include glucose production, VLDL secretion, and interference with hepatic clearance of insulin , resulting in dyslipoproteinemia, glucose intolerance, and hyperisulinemia.

Lönnqvist et al. They observed that males had a higher fat cell volume with no sex differences in the lipolytic sensitivity to β l - and β 2 -adrenoreceptor-specific agonists or in the antilipolytic effect of insulin.

However, the lipolytic β 3 -adrenoreceptor sensitivity was 12 times higher in men, and the antilipolytic α2-adrenoreceptor sensitivity was 17 times lower in men. It was concluded that in obesity, the catecholamine-induced rate of FFA mobilization from visceral fat to the portal venous system is higher in men than women.

This phenomenon is partly due to a larger fat cell volume, a decrease in the function ofα 2-adrenoceptors, and an increase in the function of β 3 -adrenoreceptors. These factors may contribute to gender-specific differences observed in the metabolic disturbances accompanied by obesity, i.

Glucocorticoid receptors. Glucocorticoid receptors, one of the most important receptors for human adipose tissue function, are involved in metabolic regulation and distribution of body fat under normal as well as pathophysiological conditions. Glucocorticoid receptors in adipose tissue show a regional variation in density with elevated concentrations in visceral adipose tissue In spite of the lower receptor density, the elevated cortisol secretion results in clearly increased net effects of cortisol.

Androgen and estrogen receptors. Adipocytes have specific receptors for androgens, with a higher density in visceral fat cells than in adipocytes isolated from subcutaneous fat. Unlike most hormones, testosterone induces an increase in the number of androgen receptors after exposure to fat cells , thereby affecting lipid mobilization.

It's found in the spaces surrounding the liver, intestines, and other organs. It's also stored in the omentum, an apron-like flap of tissue that lies under the belly muscles and blankets the intestines.

The omentum gets harder and thicker as it fills with fat. Although visceral fat makes up only a small proportion of body fat, it's a key player in a variety of health problems. As women go through their middle years, their proportion of fat to body weight tends to increase — more than it does in men — and fat storage begins favoring the upper body over the hips and thighs.

Even if you don't actually gain weight, your waistline can grow by inches as visceral fat pushes out against the abdominal wall. Visceral fat lies in the spaces between the abdominal organs and in an apron of tissue called the omentum.

Subcutaneous fat is located between the skin and the outer abdominal wall. Body fat, or adipose tissue, was once regarded as little more than a storage depot for fat blobs waiting passively to be used for energy.

But research has shown that fat cells — particularly visceral fat cells — are biologically active. One of the most important developments [since the mids] is the realization that the fat cell is an endocrine organ, secreting hormones and other molecules that have far-reaching effects on other tissues.

Before researchers recognized that fat acts as an endocrine gland, they thought that the main risk of visceral fat was influencing the production of cholesterol by releasing free fatty acids into the bloodstream and liver.

We now know that there's far more to the story. Researchers have identified a host of chemicals that link visceral fat to a surprisingly wide variety of diseases. Subcutaneous fat produces a higher proportion of beneficial molecules, and visceral fat a higher proportion of molecules with potentially deleterious health effects.

Visceral fat makes more of the proteins called cytokines, which can trigger low-level inflammation, a risk factor for heart disease and other chronic conditions. It also produces a precursor to angiotensin, a protein that causes blood vessels to constrict and blood pressure to rise.

A tape measure is your best home option for keeping tabs on visceral fat. Measure your waistline at the level of the navel — not at the narrowest part of the torso — and always measure in the same place. According to official guidelines, the bottom of the tape measure should be level with the top of the right hip bone, or ilium — see the illustration — at the point where the ilium intersects a line dropped vertically from the center of the armpit.

Don't suck in your gut or pull the tape tight enough to compress the area. In women, a waist circumference of 35 inches or larger is generally considered a sign of excess visceral fat, but that may not apply if your overall body size is large.

Rather than focus on a single reading or absolute cut-off, keep an eye on whether your waist is growing are your pants getting snug at the waist? That should give you a good idea of whether you're gaining unhealthy visceral fat. Visceral fat can be measured in a variety of ways. CT scans and full-body MRIs are the most precise, but they are expensive and rarely available, so investigators often use estimates based on waist circumference or waist size in proportion to height see "Gut check".

To ensure that they're not just measuring overall obesity, researchers also check whether a person's waist circumference is higher than average for her or his body mass index BMI. Cardiovascular disease. Several studies have documented this effect.

For example, a large study of European women ages 45 to 79 concluded that those with the biggest waists and those with the largest waists in relation to their hip size had more than double the risk of developing heart disease.

The risk was still nearly double even after adjustment for several other risk factors, including blood pressure, cholesterol, smoking, and BMI.

Higher visceral-fat volume also has a deleterious impact on several other heart disease risk factors. It's associated with higher blood pressure, blood sugar levels and triglyceride levels, and lower levels of HDL good cholesterol.

Taken together, these changes, known as metabolic syndrome, create a serious risk for cardiovascular disease and type 2 diabetes. Researchers at Kaiser Permanente found that people in their early 40s with the highest levels of abdominal fat, compared with those who had the least abdominal fat at that age, were nearly three times more likely to develop dementia including Alzheimer's disease by their mids to early 80s.

Dementia was not associated with increased thigh size. The risks were highest for women who were both large-waisted and overweight or obese. The investigators believe that belly fat raises the risk of asthma more than other poundage because it has inflammatory effects throughout the body, including in the airways.

Breast cancer. A combined analysis of several studies found that premenopausal women with abdominal obesity the largest waist size in proportion to their height were at greater risk for breast cancer.

Large waists were also linked to breast cancer risk among postmenopausal women, but that effect was not significant once BMI was taken into account. Colorectal cancer. People with the most visceral fat have three times the risk of developing colorectal adenomas precancerous polyps than those with the least visceral fat.

The list of molecules that influence browning has grown in direct proportion to the popularity of this topic and is constantly evolving as more knowledge is acquired.

Among these molecules are irisin and fibroblast growth factor 21 FGF21 , which have been well-studied and are believed to be important regulators of browning.

Irisin is secreted from muscle in response to exercise and has been shown to increase browning by acting on beige preadipocytes. In mice, it was found that beiging can occur through the production of methionine-enkephalin peptides by type 2 innate lymphoid cells in response to interleukin Due to the complex nature of adipose tissue and a growing list of browning regulatory molecules, great potential exists for the use of bioinformatics tools to improve study within this field.

Studies of WAT browning have greatly benefited from advances in these techniques, as beige fat is rapidly gaining popularity as a therapeutic target for the treatment of obesity and diabetes. DNA microarray is a bioinformatics tool used to quantify expression levels of various genes simultaneously, and has been used extensively in the study of adipose tissue.

One such study used microarray analysis in conjunction with Ingenuity IPA software to look at changes in WAT and BAT gene expression when mice were exposed to temperatures of 28 and 6 °C. It was discovered that many of the pathways upregulated in WAT after cold exposure are also highly expressed in BAT, such as oxidative phosphorylation , fatty acid metabolism , and pyruvate metabolism.

Mössenböck et al. also used microarray analysis to demonstrate that insulin deficiency inhibits the differentiation of beige adipocytes but does not disturb their capacity for browning.

RNA sequencing RNA-Seq is a powerful computational tool that allows for the quantification of RNA expression for all genes within a sample. Incorporating RNA-Seq into browning studies is of great value, as it offers better specificity, sensitivity, and a more comprehensive overview of gene expression than other methods.

RNA-Seq has been used in both human and mouse studies in an attempt characterize beige adipocytes according to their gene expression profiles and to identify potential therapeutic molecules that may induce the beige phenotype. One such study used RNA-Seq to compare gene expression profiles of WAT from wild-type WT mice and those overexpressing Early B-Cell Factor-2 EBF2.

WAT from the transgenic animals exhibited a brown fat gene program and had decreased WAT specific gene expression compared to the WT mice. Chromatin immunoprecipitation with sequencing ChIP-seq is a method used to identify protein binding sites on DNA and assess histone modifications.

This tool has enabled examination of epigenetic regulation of browning and helps elucidate the mechanisms by which protein-DNA interactions stimulate the differentiation of beige adipocytes. Studies observing the chromatin landscapes of beige adipocytes have found that adipogenesis of these cells results from the formation of cell specific chromatin landscapes, which regulate the transcriptional program and, ultimately, control differentiation.

Using ChIP-seq in conjunction with other tools, recent studies have identified over 30 transcriptional and epigenetic factors that influence beige adipocyte development.

The thrifty gene hypothesis also called the famine hypothesis states that in some populations the body would be more efficient at retaining fat in times of plenty, thereby endowing greater resistance to starvation in times of food scarcity. This hypothesis, originally advanced in the context of glucose metabolism and insulin resistance, has been discredited by physical anthropologists, physiologists, and the original proponent of the idea himself with respect to that context, although according to its developer it remains "as viable as when [it was] first advanced" in other contexts.

In , Jeffrey Friedman , in his residency at the Rockefeller University , together with Rudolph Leibel , Douglas Coleman et al. discovered the protein leptin that the genetically obese mouse lacked. When leptin levels drop, the body interprets this as a loss of energy, and hunger increases.

Mice lacking this protein eat until they are four times their normal size. Leptin, however, plays a different role in diet-induced obesity in rodents and humans.

Because adipocytes produce leptin, leptin levels are elevated in the obese. However, hunger remains, and—when leptin levels drop due to weight loss—hunger increases. The drop of leptin is better viewed as a starvation signal than the rise of leptin as a satiety signal.

The changes that occur in the hypothalamus to result in leptin resistance in obesity are currently the focus of obesity research. Gene defects in the leptin gene ob are rare in human obesity.

Several mutations of genes involving the melanocortins used in brain signaling associated with appetite and their receptors have also been identified as causing obesity in a larger portion of the population than leptin mutations.

Adipose tissue has a density of ~0. A body fat meter is a tool used to measure the body fat to weight ratio in the human body. Different meters use various methods to determine the ratio.

They tend to under-read body fat percentage. In contrast with clinical tools, one relatively inexpensive type of body fat meter uses the principle of bioelectrical impedance analysis BIA in order to determine an individual's body fat percentage. To achieve this, the meter passes a small, harmless, electric current through the body and measures the resistance , then uses information on the person's weight, height, age, and sex to calculate an approximate value for the person's body fat percentage.

The calculation measures the total volume of water in the body lean tissue and muscle contain a higher percentage of water than fat , and estimates the percentage of fat based on this information.

The result can fluctuate several percentage points depending on what has been eaten and how much water has been drunk before the analysis. Before bioelectrical impedance analysis machines were developed, there were many different ways in analyzing body composition such as skin fold methods using calipers , underwater weighing , whole body air displacement plethysmography ADP and DXA.

Within the fat adipose tissue of CCR2 deficient mice , there is an increased number of eosinophils , greater alternative Macrophage activation, and a propensity towards type 2 cytokine expression.

Furthermore, this effect was exaggerated when the mice became obese from a high fat diet. Contents move to sidebar hide. Article Talk. Read Edit View history. Tools Tools. What links here Related changes Upload file Special pages Permanent link Page information Cite this page Get shortened URL Download QR code Wikidata item.

Download as PDF Printable version. In other projects. Wikimedia Commons. Loose connective tissue composed mostly by adipocytes. For the fictional creature from Doctor Who, see List of Doctor Who universe creatures and aliens 0—9, A—G § Adipose.

See also: Fat. Adipose tissue is one of the main types of connective tissue. See also: Abdominal obesity. See also: Body fat percentage. Main article: Brown adipose tissue. Main article: Genetics of obesity § Genes.

See also: Bioelectrical impedance analysis. Stem Cells and Development. doi : PMC PMID Endocrine Reviews. The Journal of Clinical Endocrinology and Metabolism. ImmunoTargets and Therapy. Bibcode : Natur. S2CID The American Journal of Clinical Nutrition. The Fats of Life.

Cambridge University Press. ISBN Prostaglandins, Leukotrienes, and Essential Fatty Acids. Deutsches Ärzteblatt International. September Diabetes Care.

American Journal of Physiology. Endocrinology and Metabolism. International Journal of Obesity and Related Metabolic Disorders. European Journal of Nutrition. American Journal of Human Biology. Archived from the original on Retrieved See: Andrews M Yahoo Health. Women's Health.

The Brigham Intensive Review of Internal Medicine 2nd ed.

Error: This is Subcutaneous fat cells. Error: Not a valid value. Most fat is stored underneath Eco-friendly products online Subcktaneous and is Subcutaneosu as subcutaneous fat. This is the fat that is visible and that you can feel. The rest of the fat in the body is stored around your internal organs, including your heart, liver and intestines. Subcutaneous fat cells

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