Metabolic syndrome abdominal obesity -
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Despres JP, Golay A, Sjostrom L. Effects of rimonabant on metabolic risk factors in overweight patients with dyslipidemia. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide.
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Development of abdominal obesity. Abdominal obesity and elevated cardiometabolic risk. Implications for therapy. Journal Article. Abdominal obesity: the most prevalent cause of the metabolic syndrome and related cardiometabolic risk.
Jean-Pierre Després Jean-Pierre Després. Québec Heart Institute, Laval Hospital Research Center, Université Laval, , chemin Ste-Foy, Pavilion Marguerite-D'Youville, 4th Floor, Ste-Foy, Québec, Canada G1V 4G5.
E-mail address : jean-pierre. despres crhl. Oxford Academic. Google Scholar. PDF Split View Views. Select Format Select format.
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Abstract Abdominal obesity, due to intra-abdominal adiposity, drives the progression of multiple cardiometabolic risk factors independently of body mass index.
Abdominal obesity , Adiponectin , Cardiometabolic risk , Inflammation , Metabolic syndrome. Figure 1. Open in new tab Download slide. Table 1 Overview of key adipokines. Key properties. Secretion in abdominal obesity. See text for explanation and references.
Open in new tab. Figure 2. Figure 3. Figure 4. Table 2 Prognostic value of high waist circumference beyond BMI: data from an analysis of patients undergoing coronary angiography. P -value. Figure 5. a Significance vs.
b Significance vs. Int J Obes. Obes Res. Am J Clin Nutr. Am J Epidemiol. Am J Cardiol. Curr Drug Targets. Endocr Rev. Five year changes in waist circumference, body mass index and obesity in Augsburg, Germany Eur J Nutr.
Int J Epidemiol. Hypertens Res. Diabetes Res Clin Pract. PNG Med J. Curr Opin Pharmacol. Curr Diab Rep. Arterioscler Thromb Vasc Biol. Curr Cardiol Rep. Diabetes Care. J Lipid Res. J Clin Endocrinol Metab. Am J Physiol Heart Circ Physiol. Proc Natl Acad Sci USA.
Int J Obes Relat Metab Disord. Cytokine Growth Factor Rev. Am Heart Hosp J. Lancet Neurol. Arch Mal Coeur Vaiss. Elevated portal vein FFA levels with insulin resistance lead to an overproduction of apo B-containing particles.
Apo B is the structural protein of atherogenic lipoproteins, including VLDL and IDL, and the apo B concentration reflects the total number of atherogenic particles in the blood. The metabolic syndrome is associated with increased numbers of small VLDL, IDL, and LDL particles, with a decreased triglyceride to apo B ratio compared with normal.
An increased number of small, dense LDL particles is a constant feature of the dyslipidemia of abdominal adiposity, as they are associated with insulin resistance, intraabdominal fat, and hypertension 18 — LDL comprises a spectrum of particles that vary in size, density, chemical composition, and atherogenic potential.
In conditions of elevated triglycerides, LDL particles become enriched in triglycerides and depleted of core cholesteryl esters see Fig. Hepatic lipase then acts to hydrolyze these triglyceride-rich LDL, forming smaller, denser LDL particles. The presence of small, dense cholesterol-depleted LDL particles is associated with an increased risk of myocardial infarction 21 — 23 and worsened severity of CAD 24 — The Familial Atherosclerosis Treatment Study showed that the strongest predictor of coronary artery stenosis regression, induced by aggressive lipid lowering, was the increase in LDL buoyancy, not the change in LDL cholesterol level Cholesteryl ester transfer protein CETP facilitates the exchange of cholesterol ester in LDL and HDL particles for triglyceride in VLDL particles.
The transfer of triglyceride into LDL and HDL particles makes them triglyceride-rich and hence a better substrate for hepatic lipase. Elevated hepatic lipase activity leads to a predominance of small, dense LDL particles and a reduction in HDL 2 , the more antiatherogenic subspecies of HDL.
Although the mechanisms underlying the association of small, dense LDL with increased risk of CAD are not clear, several hypotheses have been proposed.
One explanation is that the presence of small, dense LDL particles is a marker of an atherogenic lipoprotein phenotype comprised of elevated triglycerides, reduced HDL, and elevated apo B, which together increase CAD risk Mechanistically, small, dense LDL particles enter the arterial wall more easily 29 , bind to arterial wall proteoglycans more avidly 30 , and are highly susceptible to oxidative modification, leading to macrophage uptake 31 , 32 , all of which may contribute to increased atherogenesis.
HDL and VLDL metabolism are closely linked, which explains why increased plasma triglyceride is almost always associated with reduced HDL levels.
Cholesteryl ester transfer protein mediates the exchange of triglyceride in VLDL for cholesteryl ester in LDL and HDL, leading to the production of triglyceride-rich LDL and HDL particles. Subsequent hepatic lipase-mediated hydrolysis of these particles leads to the generation of small, dense LDL particles and a decrease in HDL 2 cholesterol the large buoyant and antiatherogenic subspecies of total HDL; see Fig.
Many studies have shown significantly increased CAD risk with the features of the metabolic syndrome, described under different names, but until recently limited information was available about the prevalence of the syndrome in the general population 20 , 23 , 34 , It is now clear that the metabolic syndrome is very common in westernized countries and varies with age, ethnicity, and body mass index 36 — Ford et al.
Alexander et al. The presence of the metabolic syndrome is estimated to increase the risk of coronary heart disease by 1. Although individuals with the combination of the metabolic syndrome and diabetes have a high overall age-adjusted prevalence of CAD Recently published American Heart Association guidelines describe the presence of the metabolic syndrome, without diabetes, as a moderate CAD risk factor No study to date has established the contribution of familial combined hyperlipidemia to CAD risk in nondiabetic individuals with the metabolic syndrome see below.
Individuals with the combination of the metabolic syndrome MS and diabetes DM have a high overall age-adjusted prevalence of CHD, whereas the presence of the metabolic syndrome in subjects without diabetes appears to convey a moderate risk of CAD compared with those with neither The recent emphasis on treatment of the dyslipidemia of the metabolic syndrome has compelled practitioners to consider lipid-lowering therapy in a greater number of their patients, as epidemiological studies have shown that one in two individuals over 50 yr of age has the metabolic syndrome.
It is not yet clear whether all of these patients should be treated with lipid-lowering medications, and the economic impact of such a decision is enormous. Although the primary focus on CAD prevention remains on LDL lowering, LDL cholesterol levels may underestimate CAD risk in the metabolic syndrome.
Importantly, the increased event rate with the metabolic syndrome remained significant after adjustment for the Framingham yr risk score, implying independent contributions of the metabolic syndrome and the Framingham score in predicting future CAD risk The evaluation of apo B in the metabolic syndrome can help target patients for aggressive lipid-lowering therapy.
High levels of LDL cholesterol are generally accepted to be one of the strongest risk factors for CAD, but there is now significant evidence that the measurement of apo B may be an even better predictor of future CAD 45 — Insulin resistance is associated with increased numbers of small VLDL, IDL, and LDL particles, reflected by higher apo B levels, with decreased triglyceride to apo B ratios compared with those in individuals with normal insulin sensitivity.
These particles are associated with increased coronary heart disease. Studies have shown that increased apo B and apo B-containing lipoproteins VLDL and IDL are related to an increased risk of CAD 45 — 47 and that particle quantity absolute number and quality small, dense both contribute to cardiovascular risk 23 see Fig.
Bonora et al. This implies that the individuals with the metabolic syndrome had a higher number of cholesterol-deplete small, dense LDL particles. Odds ratios for ischemic heart disease IHD according to apo B levels and LDL peak particle diameter size. Men with both elevated apo B and small, dense LDL particles had a significantly higher risk of IHD than men with small, dense LDL particles but normal apo B levels.
Reprinted with permission from Lamarche et al. DM2 and FCHL share many of the phenotypic features of the metabolic syndrome increased abdominal adiposity, insulin resistance, hypertension, and dyslipidemia , but appear to convey a greater risk of CAD than the metabolic syndrome alone. Patients with DM2 are at very high risk of CAD and have been identified as candidates for aggressive lipid lowering 5 , FCHL is a common lipid disorder that shares many features of the metabolic syndrome, and most patients diagnosed with FCHL also meet the NCEP criteria for the metabolic syndrome The identification of the metabolic syndrome should prompt practitioners to further evaluate patients for DM2 or FCHL, as the diagnosis of these disorders can help target those at high risk for CAD and direct lipid-lowering therapy.
FCHL is the most common genetic form of hyperlipidemia and is associated with a 1. Goldstein et al. Although the prevalence of FCHL was originally estimated to be 0. The underlying process in FCHL appears to be the overproduction of apo B in lipoproteins VLDL, IDL, and LDL , which is not seen in other forms of hypertriglyceridemia 60 , The variable clinical lipid presentation of FCHL in patients has made their identification difficult, but the demonstration of elevated apo B and small, dense LDL particles has been shown to be a consistent feature across the variable lipid phenotypes 62 — Often one can identify affected relatives, and it is important to screen siblings and children of individuals with FCHL.
FCHL is an oligogenic disorder that is not fully expressed until the third decade of life, possibly associated with the accumulation of central abdominal fat Children who have inherited FCHL usually do not have hyperlipidemia The metabolic features of FCHL are very similar to those of the metabolic syndrome, as individuals with FCHL are also characterized by insulin resistance, increased abdominal obesity, and hypertension 65 — Hopkins et al.
Purnell et al. Further, apo B levels and small, dense LDL particles have been shown to segregate independently in families with FCHL FCHL is a subtype of the metabolic syndrome, with higher apo B levels. The identification of FCHL patients at high risk for CAD within the large population of individuals with the metabolic syndrome can help identify individuals as candidates for aggressive lipid-lowering interventions.
The metabolic syndrome is a common population trait comprised of a heterogeneous group of oligogenic disorders, such as DM2 and familial combined hyperlipidemia see Fig. The identification of these metabolic syndrome subtypes by measuring fasting glucose and apo B can help target these high risk patients for lipid-lowering therapy.
Patients with the metabolic syndrome should be screened for DM2, as individuals with DM2 and the metabolic syndrome are at high risk for CAD.
Current guidelines recommend that patients with DM2 should be aggressively treated for dyslipidemia with the goal to maintain LDL below 2. Apo B levels increase with age; therefore, age-appropriate apo B levels must be used in diagnosis Several large prospective studies have shown that the apo B level is a better predictor of future cardiovascular events than the LDL cholesterol level 45 , 71 , Recently, the Apolipoprotein-Related Mortality Risk Study published prospective data in , men and women and found that the total apo B level was a better predictor of future CAD risk than LDL cholesterol Importantly, they also found that apo B was a better predictor of CAD risk in individuals with low LDL levels, supporting the idea that patients with low LDL cholesterol levels and increased quantities of small, dense atherogenic particles VLDL, IDL, and LDL are at risk for CAD.
Apo B levels by age and gender mean and 90th percentile. To convert apo B values to grams per liter, divide by In addition to apo B, the measurement of non-HDL cholesterol total cholesterol minus HDL cholesterol can be used to assess the quantity of atherogenic apo B-containing lipoproteins VLDL, IDL, and LDL.
Some investigators have proposed that non-HDL cholesterol could replace the LDL measure in patients with hypertriglyceridemia dyslipidemia with DM2 or FCHL , because these patients have more cholesterol in VLDL particles, and LDL cholesterol alone can underestimate their CAD risk The current NCEP guidelines recommend a non-HDL cholesterol goal of less than 3.
Total apo B and non-HDL cholesterol levels are generally highly correlated, but less so at higher triglyceride levels. Comprehensive treatment of patients with the metabolic syndrome has recently been described in detail The treatment of the dyslipidemia of the metabolic syndrome should be focused on lowering LDL and apo B and increasing HDL.
Statin treatment has been shown to reduce cardiovascular events in persons with low LDL cholesterol levels at baseline The percent reduction in LDL cholesterol and apo B by statin medications is similar, but apo B may be a better marker of treatment efficacy in metabolic syndrome patients with normal LDL cholesterol Although LDL cholesterol has remained the primary target of lipid-lowering therapy, raising HDL levels is now an important secondary target to reduce CAD risk 5.
Combination lipid-lowering therapy is frequently needed to treat the dyslipidemia of the metabolic syndrome increased triglyceride, reduced HDL, and small, dense LDL particles , if lifestyle changes weight loss and exercise are inadequate.
Nicotinic acid and fibric acid derivatives both act to reduce triglyceride and increase HDL cholesterol. They are frequently used with statin medications. Although fibrate monotherapy lowers plasma triglyceride levels, it can lead to increases in LDL levels.
Bile acid resin binders lower LDL cholesterol levels, but can increase triglyceride levels in individuals susceptible to hypertriglyceridemia.
Although niacin is an inexpensive monotherapeutic agent that corrects the dyslipidemia of the metabolic syndrome, it may increase glucose levels in some patients Several groups have recently shown that niacin use in diabetic individuals was safe and effective, resulting in only a transient worsening of glycemic control 78 — The decision to initiate lipid-lowering therapy in nondiabetic individuals with the metabolic syndrome can be difficult using current guidelines, as LDL levels may underestimate CAD risk in this population.
The large population of individuals with the metabolic syndrome appears to be comprised of a heterogeneous group of disorders, and the identification of disease subtypes at high risk for CAD can help identify individuals as candidates for aggressive lipid-lowering interventions.
Two subgroups of patients with the metabolic syndrome, those with DM2 or FCHL, are at particularly high risk for premature CAD. FCHL is characterized by the metabolic syndrome in addition to a disproportionate elevation of apo B levels.
The measurement of fasting glucose and apo B in addition to the fasting lipid profile can help to estimate CAD risk and guide treatment decisions in patients with the metabolic syndrome.
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Metabolic syndrome Metabolic syndrome stroke risk associated with abdominal Metaoblic, blood lipid disorders, inflammation, syndroem Metabolic syndrome abdominal obesity or full-blown diabetes, and increased risk of Metabolic syndrome abdominal obesity cardiovascular disease. Coconut Oil Capsules criteria for identifying patients with metabolic syndrome have MMetabolic Coconut Oil Capsules abdominxl preventive medicine, but sjndrome value of syjdrome syndrome as a scientific concept remains controversial. The presence of metabolic syndrome alone cannot predict global cardiovascular disease risk. But abdominal obesity - the most prevalent manifestation of metabolic syndrome - is a marker of 'dysfunctional adipose tissue', and is of central importance in clinical diagnosis. Better risk assessment algorithms are needed to quantify diabetes and cardiovascular disease risk on a global scale. Abstract Metabolic syndrome is associated with abdominal obesity, blood lipid disorders, inflammation, insulin resistance or full-blown diabetes, and increased risk of developing cardiovascular disease.Video
Why are HDL low among individuals with abdominal obesity and the metabolic syndrome? Molly C. Carr, John D. Regional body syndrpme distribution has an ssyndrome influence on metabolic and cardiovascular Coconut Oil Capsules factors. Increased Wild salmon fishing regulations visceral fat Obesiyt is a risk factor for coronary obesiyt disease CADdyslipidemia, hypertension, stroke, and type 2 diabetes. The recent emphasis on treatment of the dyslipidemia of the metabolic syndrome hypertriglyceridemia, reduced high-density lipoprotein, and increased small, dense low-density lipoprotein particle number has compelled practitioners to consider lipid-lowering therapy in a greater number of their patients, as one in two individuals over age 50 has the metabolic syndrome.Metabolic syndrome abdominal obesity -
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Close mobile search navigation Article Navigation. Volume Article Contents Abstract. Link between abdominal obesity and metabolic abnormalities. Dyslipidemia of abdominal adiposity. Prevalence and risk of the metabolic syndrome. Metabolic syndrome: targeting high risk patients.
Screening of metabolic syndrome patients. Treatment of dyslipidemia. Journal Article. Abdominal Obesity and Dyslipidemia in the Metabolic Syndrome: Importance of Type 2 Diabetes and Familial Combined Hyperlipidemia in Coronary Artery Disease Risk.
Carr , Molly C. Carr, M. Oxford Academic. John D. PDF Split View Views. Cite Cite Molly C. Select Format Select format. ris Mendeley, Papers, Zotero. enw EndNote. bibtex BibTex. txt Medlars, RefWorks Download citation. Permissions Icon Permissions. Abstract Regional body fat distribution has an important influence on metabolic and cardiovascular risk factors.
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National Cholesterol Education Program;. National Health and Nutrition Examination Survey III;. Abdominal adipose tissue distribution, obesity, and risk of cardiovascular disease and death: 13 year follow up of participants in the study of men born in Google Scholar Crossref. Search ADS. Distribution of adipose tissue and risk of cardiovascular disease and death: a 12 year follow up of participants in the population study of women in Gothenburg, Sweden.
The pattern of subcutaneous fat distribution in middle-aged men and the risk of coronary heart disease: the Paris Prospective Study. Google Scholar PubMed.
OpenURL Placeholder Text. Definition, diagnosis and classification of diabetes mellitus and its complications. Executive summary of The third report of the National Cholesterol Education Program NCEP Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults Adult Treatment Panel III.
Sex differences in the relation of visceral adipose tissue accumulation to total body fatness. Postmenopausal hormone replacement therapy prevents central distribution of body fat after menopause. Subcutaneous and visceral adipose tissue: their relation to the metabolic syndrome.
Familial aggregation of abdominal visceral fat level: results from the Quebec family study. The growing prevalence of non-insulin-dependent diabetes in migrant Asian populations and its implications for Asia. Increased insulin resistance and insulin secretion in nondiabetic African-Americans and Hispanics compared with non-Hispanic whites.
Lipoprotein metabolism in obesity and diabetes: insights from stable isotope kinetic studies in humans. Effect of gender, age, and lipid status on low density lipoprotein subfraction distribution.
Low density lipoprotein subfractions and relationship to other risk factors for coronary artery disease in healthy individuals. Atherogenic lipoprotein phenotype.
Low-density lipoprotein subclass patterns and risk of myocardial infarction. A prospective study of triglyceride level, low-density lipoprotein particle diameter, and risk of myocardial infarction. Small, dense low-density lipoprotein particles as a predictor of risk of ischemic heart disease in men: prospective results from the Quebec Cardiovascular Study.
Relationship of low density lipoprotein subfractions to angiographically defined coronary artery disease in young survivors of myocardial infarction.
Association of small low-density lipoprotein particles with the incidence of coronary artery disease in men and women. Evidence for a new pathophysiological mechanism for coronary artery disease regression: hepatic lipase-mediated changes in LDL density.
Accumulation of lipoprotein fractions and subfractions in the arterial wall, determined in an in vitro perfusion system. Differential uptake of proteoglycan-selected subfractions of low density lipoprotein by human macrophages. Susceptibility of small, dense, low-density lipoproteins to oxidative modification in subjects with the atherogenic lipoprotein phenotype, pattern B.
Enhanced oxidative susceptibility and reduced antioxidant content of metabolic precursors of small, dense low-density lipoproteins. The role of hepatic lipase in lipoprotein metabolism and atherosclerosis.
Coronary heart disease mortality in relation with diabetes, blood glucose and plasma insulin levels. Google Scholar OpenURL Placeholder Text. Regional distribution of body fat, plasma lipoproteins, and cardiovascular disease.
Cardiovascular morbidity and mortality associated with the metabolic syndrome. The metabolic syndrome and total and cardiovascular disease mortality in middle-aged men. Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey.
The metabolic syndrome: prevalence and associated risk factor findings in the US population from the Third National Health and Nutrition Examination Survey, — NCEP-defined metabolic syndrome, diabetes, and prevalence of coronary heart disease among NHANES III participants age 50 years and older.
Prevalence and characteristics of the metabolic syndrome in the San Antonio Heart and Framingham Offspring Studies. Evidence-based guidelines for cardiovascular disease prevention in women.
Prevalence of risk factors in men with premature coronary artery disease. Apolipoprotein A-I and B levels and the risk of ischemic heart disease during a five-year follow-up of men in the Quebec cardiovascular study. Lipoprotein predictors of the severity of coronary artery disease in men and women.
High apolipoprotein B, low apolipoprotein A-I, and improvement in the prediction of fatal myocardial infarction AMORIS study : a prospective study.
Hypertriglyceridemic hyperapob: the unappreciated atherogenic dyslipoproteinemia in type 2 diabetes mellitus. Metabolic syndrome: epidemiology and more extensive phenotypic description. Coronary artery disease risk in familial combined hyperlipidemia and familial hypertriglyceridemia: a case-control comparison from the National Heart, Lung, and Blood Institute Family Heart Study.
Hyperlipidemia in coronary heart disease. Cardiovascular disease mortality in familial forms of hypertriglyceridemia: A year prospective study. Excess coronary heart disease in familial combined hyperlipidemia, in relation to genetic factors and central obesity. Inheritance of combined hyperlipoproteinemia: evidence for a new lipoprotein phenotype.
Familial lipoprotein disorders in patients with premature coronary artery disease. Very low density lipoprotein overproduction in genetic forms of hypertriglyceridaemia.
Integrated regulation of very low density lipoprotein triglyceride and apolipoprotein-B kinetics in man: normolipemic subjects, familial hypertriglyceridemia and familial combined hyperlipidemia.
Plasma lipoproteins in familial combined hyperlipidemia and monogenic familial hypertriglyceridemia. Small, dense LDL and elevated apolipoprotein B are the common characteristics for the three major lipid phenotypes of familial combined hyperlipidemia.
Diagnosis of familial combined hyperlipidemia based on lipid phenotype expression in 32 families: results of a 5-year follow-up study. Relationship of insulin sensitivity and ApoB levels to intra-abdominal fat in subjects with familial combined hyperlipidemia.
Nonobese patients with familial combined hyperlipidemia are insulin resistant compared with their nonaffected relatives. Familial dyslipidemic hypertension syndrome: familial combined hyperlipidemia, and the role of abdominal fat mass.
Increased intima-media thickness in familial combined hyperlipidemia associated with apolipoprotein B. Genetic predictors of FCHL in four large pedigrees. Apolipoprotein B and AI distributions in the United States, — results of the National Health and Nutrition Examination Survey III NHANES III.
Nonfasting apolipoprotein B and triglyceride levels as a useful predictor of coronary heart disease risk in middle-aged UK men.
Non-high-density lipoprotein cholesterol level as potential risk predictor and therapy target. Apolipoproteins versus lipids as indices of coronary risk and as targets for statin treatment. Varying cost and free nicotinic acid content in over-the-counter niacin preparations for dyslipidemia.
Effect of niacin on lipid and lipoprotein levels and glycemic control in patients with diabetes and peripheral arterial disease: the ADMIT study: a randomized trial. Efficacy, safety, and tolerability of once-daily niacin for the treatment of dyslipidemia associated with type 2 diabetes: results of the assessment of diabetes control and evaluation of the efficacy of niaspan trial.
Safety and tolerability of simvastatin plus niacin in patients with coronary artery disease and low high-density lipoprotein cholesterol The HDL Atherosclerosis Treatment Study.
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It has been suggested that exercise as a medical intervention should be prescribed in terms of its dose, i. mode, intensity, frequency and duration [ 14 ]. This was the basis of the American College of Sports Medicine Exercise is Medicine® EIM initiative [ 15 ] and their guidance on prescribing exercise [ 16 ].
The aim of this review is to i summarise current evidence on the pathophysiology of dysfunctional adipose tissue adiposopathy , its relationship to metabolic syndrome and how exercise may mediate these processes; and ii evaluate current evidence on the clinical efficacy of exercise in the management of abdominal obesity and to assess the type and dose of exercise needed for optimal improvements in health status.
To understand the significance of abdominal obesity and its contribution to metabolic syndrome, it is necessary to appreciate the link between the diseases associated with this condition. The accumulation of ectopic fat in tissue surrounding the viscera is directly related to the development of insulin resistance [ 17 ].
Insulin resistance is thought to be the common denominator in the development of metabolic syndrome. In addition, evidence suggests that systemic inflammation is an important factor in its development, through the development of insulin resistance [ 18 , 19 , 20 , 21 ]. Dysfunctional adipose tissue secretes pro-inflammatory biomarkers including prostaglandins, C-reactive protein CRP , and cytokines such as interleukins e.
interleukin-6 , tumour necrosis factor alpha TNF-α , and leptin [ 22 , 23 ]. With increasing obesity there is also a corresponding decrease in levels of adiponectin, an antiatherosclerotic adipokine [ 24 ]. Inflammatory mediators released by adipose tissue contribute to the development of type II diabetes, hyperlipidaemia and cardiovascular disease [ 25 , 26 ].
If there is a high proportion of fat to muscle this is likely to contribute to this metabolic dysfunction as an increase in circulation of free fatty acids requires greater insulin secretion for control of glucose metabolism. The resulting hyperinsulinaemia desensitises insulin-sensitive tissues, which predisposes individuals to type II diabetes [ 27 ].
The decrease in adiponectin secretion also inhibits insulin receptor proteins. Moreover, regular consumption of foods rich in carbohydrate results in postprandial hyperglycaemia which causes repetitive acute inflammation which might contribute to a chronic inflammatory state [ 28 ]. Chronic systemic inflammation increases oxidative stress and reduces metabolic flexibility, thus perpetuating metabolic syndrome, leading to a vicious cycle of disease, depression and further inactivity [ 29 , 30 ].
Adipose tissue hypoxia also occurs in the obese state although the mechanisms for this are not fully understood [ 19 ]. It has been suggested that deficient angiogenesis causes decreased blood flow due to reduction in capillary density and excessive growth of adipose tissue.
This may also be exacerbated by obstructive sleep apnoea which is common in obese individuals, and results in a reduction of oxygen to the tissues [ 31 ]. Adipose tissue, hypoxia is associated with an increased expression of inflammatory genes and decreased expression of adiponectin, resulting in local and systemic inflammation [ 19 , 32 , 33 ].
The response to adipose tissue hypoxia includes insulin sensitivity and glucose intolerance as adiponectin is associated with normal glucose and lipid metabolism. Leptin expression has also been shown to increase in obesity and the likely explanation for this is adipose tissue hypoxia [ 34 ].
This is important as leptin expression modulates insulin resistance [ 35 ]. Furthermore, ghrelin regulation in obese individuals is affected and serum ghrelin suppression in response to stomach fullness is impaired which results in a failure to suppress the continued desire to eat, thus compounding the problem [ 35 ].
Hypothlamic-pituitary-adrenal HPA axis hyperactivity is evident in abdominal obesity and is also associated with insulin resistance due to an increase in cortisol levels [ 36 ].
Cortisol, secreted by the adrenal glands, is involved in glucogenesis which increases blood sugar as a response to stress. Epidemiological data provide evidence for a significant positive association between increased cortisol levels and the risk of developing type II diabetes and atherosclerosis due to a failure to suppress inflammation [ 37 ].
Also, the secretion of low grade inflammatory mediators by adipose tissues may act as an additional chronic stimulus to the activation of the HPA axis which in turn results in increased levels of cortisol secretion, resulting in a positive feedback loop [ 38 ].
At present, there is no explanation for this and it is not known whether these metabolically healthy obese individuals will eventually develop metabolic syndrome and are simply experiencing a delayed-onset of disease [ 24 ].
When BMI is used as a measure of obesity only a modest association with cardiovascular risk factors is found [ 18 ]. However, when abdominal obesity measurements, such as waist circumference or waist:hip ratio are included as a measure of abdominal adiposity a strong association with cardiovascular and metabolic syndrome risk factors is found [ 42 , 43 , 44 , 45 ].
Abdominal adiposity is a reversible condition and its reduction can have excellent effects in diminishing cardiovascular and metabolic syndrome risk. Evidence from a study by Brooks, et al.
demonstrated that increased abdominal obesity was associated with systemic inflammation as measured by high-sensitivity C-reactive protein hsCRP [ 18 ]. Given the direct link between abdominal obesity and systemic inflammation it is not surprising that even modest reductions in abdominal adipose tissue are accompanied by improvements in metabolic function and reduced cardiovascular risk.
Several studies show a strong association between obesity and physical inactivity [ 46 , 47 , 48 ] and that metabolic syndrome is associated with sedentary lifestyle and poor cardiorespiratory fitness [ 49 ].
Sedentary behaviour is widely regarded as activity which involves energy expenditure at the level of 1. Edwardson et al. conducted a meta-analysis that found that individuals who spend more time in sedentary behaviours have greater odds of having metabolic syndrome [ 50 ]. A longitudinal study observing adults found that improvements in cardiometabolic factors occurred in overweight and obese individuals with increased levels of physical activity, although the participants were those participating in a health screening programme and were therefore probably of a higher economic status.
At follow-up, there was a statistically significant decrease in non-HDL concentrations of 5. Of the parameters observed, non-HDL cholesterol and plasma triglycerides were found to have the largest improvement when physical activity was increased. A study followed 22, participants, aged 30—64 years, comparing metabolic syndrome risk with intensity level of leisure-time exercise and by occupational and commuting activity [ 53 ].
Leisure-time activity was found to be linearly and inversely associated with a risk of developing metabolic syndrome and vigorous-intensity activity alone or a combination of both moderate- and vigorous-intensity activity was associated with a lower risk of metabolic syndrome.
The introduction of increased physical activity into a previously inactive lifestyle might also break the cycle of inflammation-mediated sickness behaviour as described by Nunn, which suppresses the desire to undertake physical activity [ 30 ].
A systematic review and meta-analysis was conducted by Ostman et al. A total of 16 studies participants were included in the review and it was found that aerobic training produced small improvements in fasting blood glucose, triglycerides and low-density lipoproteins.
Nevertheless, combined with improvements in maximal oxygen uptake and blood pressure, the overall risk profile for patients was much improved.
The improvements in waist measurement would suggest that the long-term risks associated with metabolic syndrome were reduced. There are a number of studies which have specifically investigated the effect of exercise on abdominal obesity, irrespective of total body weight and these are summarised in a comprehensive review by Pedersen and Saltin [ 56 ].
Amongst their findings they reported that a cross-sectional study of overweight males showed that those with a high level of fitness as measured by activity and maximal oxygen uptake had lower levels of visceral fat than their unfit counterparts when scanned using magnetic resonance imaging [ 39 ].
Lee et al. investigated the effects of exercise without weight loss on total and abdominal adiposity and skeletal muscle mass and composition in previously sedentary, lean men and in obese men with and without type II diabetes [ 11 ].
It was found that, even in the absence of weight loss, moderate-intensity exercise was associated with significant reductions in total and abdominal fat, and there was a reduction in skeletal muscle lipid content independent of group.
Stewart et al. investigated the effects of exercise on cardiovascular and metabolic disease in older adults and found that reductions in total and abdominal fatness and increase in leanness were strongly associated with reductions in risk factors for cardiovascular disease and diabetes, including those that constitute metabolic syndrome [ 57 ].
conducted a longitudinal study of 32, adults who underwent an abdominal computerised tomography scan as part of health screening and found that the ratio of visceral-to-subcutaneous fat was independently associated with all-cause mortality.
This suggests that the location of fat deposits in the abdomen viscera is a better indicator of metabolic risk than total body fat, which is unsurprising given the positive association between abdominal adiposity and systemic inflammation [ 58 ]. A number of reviews have shown that exercise training specifically elicits an anti-inflammatory effect, independent of weight loss [ 33 , 59 , 60 , 61 , 62 ].
Other metabolic benefits of exercise were reported in a study on patients with type II diabetes where pedometer-measured exercise was not only associated with reductions in systemic inflammation, but also reductions in abdominal obesity and arterial stiffness [ 63 ].
One of the mechanisms for the anti-inflammatory effect of exercise is a reduction in adipose tissue hypoxia resulting from improved capillary density blood flow. In a review by Golbidi [ 24 ] the inverse relationship between exercise, body mass index BMI , hip-waist ratio, and waist circumference was described.
The anti-inflammatory effect of exercise was also explained as being closely related to oxidative stress.
Exercise was shown to improve glucose tolerance, insulin resistance and lipid metabolism and reduce blood pressure in both healthy individuals and those with metabolic disease. Large population cohort studies observed relationships between plasma CRP and the level of exercise that was independent of obesity as measured by body mass index [ 62 , 64 ].
The effect of exercise training on CRP was investigated in a systematic review which considered a total of 83 studies of different types.
It was found that exercise training led to a greater reduction in CRP when accompanied by a decrease in BMI, but that significant reductions in CRP occurred without weight loss [ 65 ].
Furthermore, a Cochrane review provided evidence that exercise improved general health even where no weight was lost because it improved plasma lipoprotein profile [ 66 ]. Not all studies provide evidence that exercise training reduces pro-inflammatory biomarkers.
Melo et al. reviewed 11 studies of patients with type II diabetes and found insufficient evidence to determine whether aerobic or resistance exercise improved systemic levels of inflammatory markers [ 67 ]. However, an earlier review by Hayashino et al.
found that both CRP and IL-6 were reduced by exercise training [ 68 ]. It is still unclear whether improvements in inflammatory status are independent of weight loss or entirely dependent upon the changes in body composition that result from exercise training [ 61 ].
Nevertheless, Eaton and Eaton observed that the percentage of lean body mass is critical in avoiding the hyperinsulinaemia which predisposes individuals to type II diabetes because a greater insulin secretion is required for any given glucose load where levels of body fat are disproportionate [ 27 ].
This would suggest that strength training that develops lean tissue is critical in the treatment, or prevention, of metabolic disease. There are no specific guidelines on exercise prescription for systemic inflammation although guidance is available in the form of programmes designed to reduce body fat and improve general health status.
The American College of Sports Medicine ACSM recommends — min of moderate-intensity exercise per week as optimal but other authors have suggested between 30 [ 69 ] and 60 [ 70 ] minutes per day would be required.
A systematic review and meta-analysis by Hayashino et al. They found that exercise training with a longer duration and frequency was more effective in reducing systemic inflammation, suggesting that these effects might be dose-dependent.
More recently, this idea has been challenged and it is now thought that shorter-duration, higher intensity interval training HIIT is beneficial [ 76 ]. Recent findings suggest that HIIT programmes are effective in reducing metabolic syndrome combined with high adherence rates and this is important because incorporating HIIT programmes into daily life is less disruptive.
Gremeaux, et al. studied the effects of HIIT training on a sample of 62 overweight or obese adults who were above the recommended abdominal obesity threshold. It was found that the prevalence of metabolic syndrome was reduced by The metabolic and vascular effects of these three different regimens were studied and improvements were observed in various measures including BMI, waist measurement, glucose metabolism, insulin resistance and lipid profiles.
Zhang et al. also found that high intensity interval training was better than continuous moderate aerobic training in reducing abdominal visceral fat in obese young women [ 78 ]. Similar findings from other studies support the benefit of high-intensity interval training performed in short, high-intensity bursts, involving as little as 10 min of activity at a time, and this might promote better adherence in non-habitual exercisers [ 79 , 80 , 81 ].
A further study of adults found that consistent moderate to vigorous activity was more important than exercise volume in reducing CRP levels associated with systemic inflammation [ 82 ]. A systematic review by Cronin et al.
found that greater reductions in inflammatory biomarkers occurred in older healthy inactive participants when higher intensity aerobic exercise was undertaken [ 83 ]. A review by Zdziarski et al. found that largest reductions in systemic inflammation and improvements in well-being, depression and sleep was achieved using multi-modal exercise aerobic and resistance training in individuals with inflammation-related chronic pain [ 84 ].
This is important because it is likely that individuals in a pro-inflammatory state due to abdominal adiposopathy may also be susceptible to chronic pain conditions. Dutheil et al. reported that high resistance-moderate endurance training was efficient in improving visceral fat loss in healthy adults [ 85 ].
If changes in body composition are more important than total body weight loss then resistance training combined with aerobic exercise would produce optimal effects in increasing percentage lean body mass [ 27 ].
One of the major challenges in using programmes of exercise to improve health status is promoting and maintaining adherence in individuals who have often been inactive for many years and who may be overweight or obese [ 86 ].
To promote adherence Clauw and Crofford suggested that additional activity is incorporated very gradually — as little as 5 min daily [ 88 ] although the programme needs to be tailored to the individual whilst aiming to deliver optimal effects [ 84 ].
As discussed above, the recent findings that HIIT programmes are effective in reducing metabolic syndrome combined with high adherence rates is significant because incorporating it into daily life is less disruptive.
Connelly et al. conducted a review to assess the effectiveness of technology to promote physical activity in people with Type 2 diabetes and found that the use of technology-based interventions, such as mobile phone applications, texts and email support, improves compliance [ 89 ].
In summary, evidence suggests that optimal abdominal fat reduction and the development of lean tissue is achieved by combining high-intensity interval training and resistance training with an overall general increase in daily physical activity. An increasingly sedentary lifestyle, a lack of regular exercise and an increase in obesity have been the main contributors to a rise in the incidence of metabolic dysfunction, particularly in the developed world.
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Abdominal abdomnial, due to intra-abdominal adiposity, drives the progression obesith multiple cardiometabolic risk factors independently of Coconut Oil Capsules Inflammation and wound healing Coconut Oil Capsules. Abxominal occurs both through altered secretion Mteabolic adipocyte-derived Coconut Oil Capsules active substances adipokinessyndro,e free fatty acids, adiponectin, interleukin-6, tumour Coconut Oil Capsules factor alpha, and plasminogen activator inhibitor-1, and through exacerbation of insulin resistance and associated cardiometabolic risk factors. The prevalence of abdominal obesity is increasing in western populations, due to a combination of low physical activity and high-energy diets, and also in developing countries, where it is associated with the urbanization of populations. The measurement of waist circumference, together with an additional comorbidity, readily identifies the presence of increased cardiometabolic risk associated with abdominal obesity. Accordingly, measurement of waist circumference should become a standard component of cardiovascular risk evaluation in routine clinical practice.
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