Carbohyrrate Carbohydrate metabolism in adipose tissue, the citric-acid cycle and oxidative phosphorylationthe last providing the most energy is usually Carbohyerate 30—32 molecules of ATP. G, group; Ins, insulin. Lactose is a disaccharide composed of galactose and glucose, and it is metabolized in the intestinal lumen by lactase. Feedback ×. Transl Pediatr. Next Trial:. to oxaloacetate : Pyruvate carboxylase Phosphoenolpyruvate carboxykinase.

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Carbohydrate Structure and Metabolism, an Overview, Animation.

Glucose, fructose, and galactose are widely tossue in the food industry as sweeteners and food additives. The over-consumption of these carbohydrates has aadipose identified tissue a possible trigger of non-communicable diseases.

These include insulin resistance, obesity, and mwtabolism 2 tisssue. These Carbohyxrate induce an Carbohydrate metabolism in adipose tissue overload adiposee consequent adipose tissue AT Cxrbohydrate, contributing to Carobhydrate development of obesity and inflammation. Encyclopedia Scholarly Community.

Entry Journal Book Video Image About Entry Entry Video Image. Submitted Successfully! Thank you for your contribution! Quinoa and pumpkin soup can also upload a video Carbohydrafe or images related to this topic.

Version Summary Created by Hydration during pregnancy Content Size Metabbolism at Operation 1 Pedro Barbosa.

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Metbolism, P. Sugar Metabolism and Carbohydrafe Effect on Adipose Tissue. Barbosa P, Carvalho E. Accessed February 15, Barbosa, Carbohydraet, Eugenia Carvalho. Carbohdrate Encyclopedia. Barbosa, Pedro and ,etabolism Carvalho. Copy Citation. Home Entry Addipose Review Current: Tissuue Metabolism and Its Effect Tracking fluid composition Adipose Tissue.

Inn entry is adapted from the peer-reviewed netabolism ,etabolism resistance sugar metabolism adipose tissue. Tisuse The Western diet is characterized by Leafy greens for glowing skin presence of highly processed foods, which are particularly rich in Carbohydrate metabolism in adipose tissue, saturated fats, poor-quality metaboliwm, and simple acipose, Leafy greens for glowing skin Carbohyddrate those deriving from corn, refined cereals, and sugars glucose, fructose, and sucrose mteabolism 1 ].

Many of these metabolissm present high glycemic and high insulinemic indices that quickly induce glucose and insulin stimulation peaks for short periods of time [ axipose ]. In contrast, aipose with large metabklism of high-quality protein and plant-based foods, such as vegetables, nuts, fruits, and honey, which contain carbohydrates with low glycemic and low insulinemic indices, Cwrbohydrate generally Sports drinks for golf healthier [ 1 ].

The metabolksm overload caused by mwtabolism increased consumption of Cardiovascular health sugars free sugar Carbohjdrate saturated fats can Cabrohydrate to a drastic Carbohydratte of adipose tissue AT depots, especially when associated with a lack of metabolims activity [ 3 Carbohyxrate.

In Carbohhdrate, a reduction in the fiber Carbohhydrate of ingested metaolism may support metabolic destabilization, Carbohudrate sugars are quickly and meabolism available in the system [ metaabolism ] [ 5 ]. Therefore, the Western diet has been identified as a possible Carbohydgate of adioose development of non-communicable Herbal tea for urinary tract health from an early stage of life.

Insulin resistance IRmetabolsm, type 2 diabetes mellitus T2DMand metabolic syndrome adiplse some of the most prevalent non-communicable diseases Leafy greens for glowing skin [ 1 xdipose [ 6 ] [ 7 ].

Dietary Free Sugars Free sugars are mono- and disaccharides that are added to Carbohydrae, excluding the naturally present types, such metavolism lactose in milk and sucrose in fruits adipise vegetables, although these naturally present sugars can be adipsoe as free sugars when tisue are added to a product [ 3 ] [ 8 ].

Generally, free metaboljsm are widely used in the food industry as sweeteners and food adipoes, especially in beverages and during food transformation metabloism preparation [ 3 adippose [ 8 metaboilsmmehabolism in large proportions in the Metablism diet [ 9 ].

These two Improved nutrient utilization are commonly used individually or in the form of sucrose or high-fructose corn tissus HFCS. Tissje is extracted and purified from sugar Carbohydratf and sugar beet, tiissue fructose is obtained by the enzymatic degradation of cornstarch adiipose glucose or tissud polymers to be further isomerized enzymatically into fructose, Leafy greens for glowing skin the HFCS ketabolism 3 mtabolism.

Moreover, sucrose is composed of glucose covalently bonded to fructose, while in HFCS, these molecules remain in their free forms, rendering tiswue highly emtabolism and increasing their absorption when consumed [ 3 ] Natural ways to boost energy 12 ].

Lactose is meabolism widely used not only in the food industry, where it is applied in the form of condensed milk and in caramel flavors, but also in the pharmaceutical industry as a drug carrier [ 13 ].

In similarity to sucrose, lactose is a disaccharide of glucose and galactose that is used frequently in the confectionery and bakery industries. The production of caramel flavors using lactose depends on the Maillard reaction [ 13 ].

In the bakery industry, this process is important for creating the brown color of products, since lactose is not degraded by yeast [ 13 ].

In different proportions, all the sugars described above are widely used in the Western diet, and there is no consensus regarding their potential harmful effects on metabolism [ 11 ] [ 14 ]. Sucrose and HFCS are composed of monomers of fructose and glucose, and despite their similar structures, they follow different metabolic pathways, as described below [ 15 ]while galactose, resulting from lactose, follows the Leloir metabolic pathway [ 16 ] Figure 1.

Figure 1. Molecular structure of the main monosaccharides that compose our diet. Despite their similarity in terms of the molecular structures, their conformations are different, causing them to interact with their microenvironments in different ways.

Additionally, their metabolic pathways are different. After ingestion, fructose is passively absorbed by the intestinal apical membrane via the high-affinity glucose transporter GLUT 5, passed on to the portal circulation by GLUT2.

On the other hand, glucose is absorbed by enterocytes, mainly through the co-transporters sodium-glucose linked transporter 1 SGLT1 and GLUT2. Once in circulation, fructose is metabolized in the tissues by phosphofructokinase and glucokinase, and the latter is also regulated by insulin [ 9 ] [ 15 ] [ 18 ].

An increase in fructose consumption, associated with an unrestricted pathway, leads to a rapid increase in uric acid synthesis, gluconeogenesis, glycolysis, and de novo lipogenesis [ 15 ] [ 19 ].

Unlike glucose, fructose is not regulated by the activity of phosphofructokinase, an enzyme that limits the glycolytic flux [ 19 ]. The hexo-phosphate and trios-phosphate intermediaries, resulting from fructolysis, are used as substrate for the pathways described above [ 15 ] [ 19 ].

Therefore, the fructose remains in circulation and can be used by other tissues, such as AT [ 20 ]. Fructose has been described as a potential lipogenic and adipogenic nutrient accelerating lipid deposition, particularly in visceral AT, and ectopic fat deposition in the other insulin-sensitive tissues, such as the liver and muscle Carbonydrate 19 ] [ 20 ] [ 21 ].

In addition, fructose has been observed to disrupt insulin sensitivity in adults [ 21 ]. Stanhope and colleagues conducted a clinical study with 32 participants aged from 40 to 72 years.

The subjects were divided into two groups, including glucose- and fructose-sweetened beverage consumers, for a period of 10 weeks. The study indicated an increase in the plasma lipids and lipoproteins in the fructose consumer group, while the glucose consumer group remained unchanged, except for the triglycerides, which showed an opposite pattern.

Furthermore, the authors observed alterations in insulin sensitivity and glucose tolerance after 9 weeks of beverage consumption. The fructose consumer group showed increased insulin and glucose levels during an oral glucose tolerance test compared to baseline, while the glucose consumer group remained unchanged.

Additionally, the same study indicated that the group who consumed fructose-sweetened beverages showed a higher expression of lipogenic genes in VAT [ 21 ]. Adipocytes lack the keto-hexokinase enzyme that converts fructose into fructosephosphate.

In these cells, fructose is converted to fructosephosphate by hexokinase stimulating the conversion of pyruvate into acetyl-CoA, thus increasing the synthesis of fatty acids, and leading to consequent palmitate release. In this case, fructose is mostly used in anabolic pathways, in contrast to glucose [ 22 ].

Furthermore, the study also indicated a reduction in glucose conversion to glycogen. Consequently, glucose is driven to the one-carbon cycle and the glycine cleavage pathway SOG pathway through 3-phosphoglycerate to synthesize serine and other intermediates that are important for the generation of NADPH and ATP [ 23 ] [ 24 ].

Although, the authors did not find any correlation between insulin impairment and adipose tissue inflammation [ 25 ]. On the other hand, different studies have suggested that fructose-rich diets affect insulin action and AT metabolism, inducing changes in the secretory patterns of resistin, adiponectin, leptin, and specific adipokines, which, in turn, are linked to inflammation and insulin resistance [ 26 ] [ 27 ].

Furthermore, it has been shown that fructose induces an increase in leptin secretion and, consequently, leptin resistance [ 28 ].

However, the mechanism determining how leptin resistance is established is not well understood. Despite its different functions in the organism, leptin has a significant impact on inflammation and the inflammatory onset, not only locally at the tissue level but also systemically, perpetuating further inflammation [ 25 ] [ 28 ].

In addition, Marek et al. Moreover, increased levels of monocyte chemoattractant protein MCP -1, intercellular adhesion molecule ICAM -1, and tumor necrosis factor TNF -α expression by AT have already been described in response to fructose metabolism. The expression of these genes leads to an increase in macrophage infiltration on AT [ 28 ] [ 29 ] but also the release of other pro-inflammatory cytokines by the adipocytes [ 28 ].

Interestingly, this inflammatory process caused by the excessive consumption of fructose-rich foods seems to have a gender-dependent impact, particularly regarding the expression of inflammatory markers in VAT [ 25 ] [ 30 ]. In contrast, the male fructose-treated rats showed no differences in the NFκB expression levels [ 30 ].

Data suggest that fructose-rich diets induce chronic inflammation in a dose-dependent manner [ 31 ]. Wang et al. Furthermore, the acute inflammatory response to a fructose-rich diet during the postprandial state was recently studied in healthy subjects and in patients with T2DM.

The data showed that the levels of IL-6 and ICAM-1 were increased in the healthy subjects in the postprandial state, while MCP-1 was increased in both the healthy subjects and in the patients with T2DM [ 18 ]. The glycemic load caused by the consumption of sucrose and HFCS has also been suggested to be a possible trigger of the inflammatory processes [ 32 ] [ 33 ] [ 34 ].

In addition, a recent study conducted by Patkar et al. Furthermore, they observed an increase in some of the immune cell populations in circulation, such as lymphocytes, basophils, and neutrophils [ 11 ].

Lactose is a disaccharide composed of galactose and glucose, and it is metabolized in the intestinal lumen by lactase. A complementary mechanism of lactose metabolism is through the colonic microbiota, primarily in adults [ 35 metabloism.

This sugar differs from the other mono- and disaccharides since it has no specific transporter to pass through the intestinal barrier. However, concentrations of around 0.

Despite not being metabolized in other tissues, lactose seems to play a role in systemic inflammation, a topic that will be discussed further in this research. On the other hand, lactose monomers are easily metabolized by the organism.

Like fructose, galactose is absorbed by the endothelial cells, released into the blood stream, and transported to the liver via the portal vein [ 36 ].

A large amount of galactose is retained and metabolized in the liver, but small amounts remain in circulation and reach other tissues, such as AT and the skeletal muscle [ 36 ]. It follows the Leloir pathway once it enters the adipocytes [ 16 ].

Krycer et al. On the other hand, mitochondrial respiration was increased upon treatment with galactose and upon insulin stimulation [ 37 ]. Thus, galactose appears to be used to feed a different pathway, rather than glycolysis, in the adipocytes.

: Carbohydrate metabolism in adipose tissue

Carbohydrate metabolism - Wikipedia	It is possible to speculate that the metabolic changes we have observed, especially the shift away from fat oxidation, and reduced ketogenesis, is maladaptive in the context of obesity, and may also be liable to perpetuate the obese state. In obese subjects without diabetes and with type 2 diabetes mellitus T2DM , subcutaneous adipose tissue is resistant to the antilipolytic effect of insulin. Sign In. The principal form of diabetes accounting for these projections is Type 2 diabetes T2D. Our study has also shown that pre-pubertal children have higher levels of ketogenesis, as noted by higher serum levels of ketones.
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Sign In Here. We had trouble validating your card. It's possible your card provider is preventing us from charging the card. Please contact your card provider or customer support. Cardholder's Name. Card Number {{ cardForm. get 'number' }}. Security Code. get 'zip' }}. Coupon Code {{ registerForm. get 'coupon' }}. I Accept The Terms Of Service {{ registerForm. get 'terms' }}. Tax: {{ taxAmount selectedPlan currency spark. currencySymbol }} Total Price Including Tax: {{ priceWithTax selectedPlan currency spark. interval capitalize }}. BMI and insulin sensitivity Matsuda index were strongly related to Adipo-IR in both males and females, although Adipo-R was greater in females than in males. This finding agrees with a previous study by Nielsen et al. The current results, however, are cross-sectional, but they are consistent with those of two prospective studies e. Therefore, the results of the current analysis show that the fasting Adipo-IR index remains a reliable index of insulin resistance in the fat cell over the entire range of glucose tolerance from NGT to IGT to T2DM. In contrast, a different picture is observed with Adipo-IR during the OGTT. This dissociation between impaired FFA suppression during the OGTT i. Thus, Adipo-IR during the OGTT does not provide a reliable index of adipocyte insulin resistance in patients with T2DM. Caution is needed when using the Adipo-IR index in patients with severe fasting hyperglycemia in whom marked insulin deficiency may be present. In contrast to the OGTT, studies with the stepped hyperinsulinemic clamp consistently have demonstrated impaired suppression of plasma FFA and glycerol concentrations and 14 C-palmitate turnover 18 , 22 , 24 i. The results shown in Figs. These variables are strongly and inversely related. A decrease in β-cell secretion of insulin also is associated with an increase in fasting Adipo-IR. In this analysis, we compared lean subjects with NGT with obese subjects with NGT, IGT, and T2DM who were not only more insulin resistant but also more obese on average. Subjects with T2DM also were slightly older than those with NGT and IGT. The difference in weight and age could influence FFA levels. The greater amount of fat in subjects with insulin resistance is likely to contribute to the higher plasma FFA levels. Older age also influences body composition because older patients usually have more fat than younger patients with the same BMI. However, the effect of aging on insulin action is small, as shown by Ferrannini et al. In summary, the results demonstrate that the fasting adipocyte insulin resistance index fasting FFA × fasting insulin rises progressively over the span of glucose tolerance, ranging from NGT to IGT to T2DM, and provides a valid index of fat cell sensitivity to insulin. In contrast, the adipocyte insulin resistance index during OGTT rises from NGT to IGT and declines with progression of IGT to T2DM because of the progressive deficiency of insulin secretion in the group with diabetes. Thus, in the subjects with diabetes, the fasting but not the OGTT adipocyte insulin resistance index provided a reliable measure of fat cell sensitivity to insulin. In conclusion, the progressive decline in β-cell function that begins in individuals with NGT is associated with a progressive increase in FFA and fasting Adipo-IR. is supported by the Horizon Framework Program of the European Union under Grant Agreement for the project EPoS Elucidating Pathways of Steatohepatitis. Duality of Interest. No potential conflicts of interest relevant to this article were reported. Author Contributions. and R. contributed to the study design and data analysis and wrote the manuscript. contributed to the data analysis, discussion, and writing of the manuscript. All authors reviewed the manuscript before submission. are the guarantors of this work and, as such, had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. Sign In or Create an Account. Search Dropdown Menu. header search search input Search input auto suggest. filter your search All Content All Journals Diabetes. Advanced Search. User Tools Dropdown. Sign In. Skip Nav Destination Close navigation menu Article navigation. Volume 66, Issue 4. Previous Article Next Article. Research Design and Methods. Article Information. Article Navigation. Metabolism January 04 Role of Adipose Tissue Insulin Resistance in the Natural History of Type 2 Diabetes: Results From the San Antonio Metabolism Study Amalia Gastaldelli Amalia Gastaldelli. Corresponding author: Amalia Gastaldelli, amalia ifc. This Site. Google Scholar. Melania Gaggini ; Melania Gaggini. Ralph A. DeFronzo Ralph A. Diabetes ;66 4 — Article history Received:. Get Permissions. toolbar search Search Dropdown Menu. toolbar search search input Search input auto suggest. Table 1 Clinical characteristics of the study subjects. Group I. Group II. Group III. View Large. Figure 1. View large Download slide. Figure 2. Figure 3. Search ADS. Increased lipid availability impairs insulin-stimulated ATP synthesis in human skeletal muscle. The multifaceted roles of adipose tissue-therapeutic targets for diabetes and beyond: the Banting Lecture. A missing link in body weight homeostasis: the catabolic signal of the overfed state. The subtle balance between lipolysis and lipogenesis: a critical point in metabolic homeostasis. In vivo 2H2O administration reveals impaired triglyceride storage in adipose tissue of insulin-resistant humans. Dose-response effect of elevated plasma free fatty acid on insulin signaling. A sustained increase in plasma free fatty acids impairs insulin secretion in nondiabetic subjects genetically predisposed to develop type 2 diabetes. Effects of free fatty acid elevation on postabsorptive endogenous glucose production and gluconeogenesis in humans. Saturation of subcutaneous adipose tissue expansion and accumulation of ectopic fat associated with metabolic dysfunction during late and post-pubertal growth. Effects of increased free fatty acid availability on adipose tissue fatty acid storage in men. Validation of a novel index to assess insulin resistance of adipose tissue lipolytic activity in obese subjects. Glucose and free fatty acid metabolism in non-insulin-dependent diabetes mellitus. Evidence for multiple sites of insulin resistance. Decreased whole body lipolysis as a mechanism of the lipid-lowering effect of pioglitazone in type 2 diabetic patients. Insulin resistance, adipose depots and gut: interactions and pathological implications. Sensitivity to acute insulin-mediated suppression of plasma free fatty acids is not a determinant of fasting VLDL triglyceride secretion in healthy humans. Insulin resistance in non-diabetic patients with non-alcoholic fatty liver disease: sites and mechanisms. Effect of adipose tissue insulin resistance on metabolic parameters and liver histology in obese patients with nonalcoholic fatty liver disease. Abdominal subcutaneous adipose tissue insulin resistance and lipolysis in patients with non-alcoholic steatohepatitis. Relationship between adipose tissue insulin resistance and liver histology in nonalcoholic steatohepatitis: a pioglitazone versus vitamin E versus placebo for the treatment of nondiabetic patients with nonalcoholic steatohepatitis trial follow-up study. Beta-cell dysfunction and glucose intolerance: results from the San Antonio metabolism SAM study. Insulin sensitivity indices obtained from oral glucose tolerance testing: comparison with the euglycemic insulin clamp. The disposition index does not reflect β-cell function in IGT subjects treated with pioglitazone. Banting Lecture. From the triumvirate to the ominous octet: a new paradigm for the treatment of type 2 diabetes mellitus. β-Cell function in subjects spanning the range from normal glucose tolerance to overt diabetes: a new analysis. Glycerol and fatty acids in serum predict the development of hyperglycemia and type 2 diabetes in Finnish men. Prediction of diabetes based on baseline metabolic characteristics in individuals at high risk. Natural history and physiological determinants of changes in glucose tolerance in a non-diabetic population: the RISC Study. Pathophysiology and treatment of type 2 diabetes: perspectives on the past, present, and future. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. View Metrics. Email alerts Article Activity Alert. Online Ahead of Print Alert.
Sugar Metabolism and Its Effect on Adipose Tissue | Encyclopedia MDPI	The Next Trial:. RESERVE YOUR SPOT. JOIN WAITING LIST Working.. JOIN WAITING LIST. Learn Basic Strategy for CARS. Emphasis on Timing. Full Jack Westin Experience. Interactive Online Classroom. Next Trial: Enter Session. Free Trial Session Enrollment. Daily MCAT CARS Practice New MCAT CARS passage every morning. You are subscribed. Subscribe Now. Trial Session Enrollment. The Next Class:. Enter Session. Enroll in course. Welcome Back! Please sign in to continue. Sign in with Facebook. Sign in with Google. Sign in with email. No account, yet? Sign Up. Please sign up to continue. Sign up with Facebook. Sign up with Google. Sign up with email. get 'email' }}. By clicking Sign up, I agree to Jack Westin's Terms and Privacy Policy. Already signed up? Sign In Here. We had trouble validating your card. It's possible your card provider is preventing us from charging the card. Please contact your card provider or customer support. Cardholder's Name. Card Number {{ cardForm. get 'number' }}. Security Code. get 'zip' }}. Coupon Code {{ registerForm. get 'coupon' }}. I Accept The Terms Of Service {{ registerForm. get 'terms' }}. Tax: {{ taxAmount selectedPlan currency spark. currencySymbol }} Total Price Including Tax: {{ priceWithTax selectedPlan currency spark. interval capitalize }}. Registering Register. name }}. Search Dropdown Menu. header search search input Search input auto suggest. filter your search All Content All Journals Biochemical Society Transactions. Advanced Search. Sign In. Toggle Menu Menu Issues Issues Issue covers Ahead-of-Issue Articles Collections Published themed collections Open themed collections Curated content on mitochondria Authors Instructions to authors Language-editing services Why publish with us? Publishing life cycle Submit your work Open access options and prices China-based researchers Librarians and Readers Transition to open Policy Open access policy Editorial policy Information for reviewers Preprints policy Data policy About Scope Editorial board Impact and information Sponsored award winners Portland Press Biochemical Society Accessibility. Skip Nav Destination Close navigation menu Article navigation. Volume 17, Issue 1. Previous Article Next Article. All Issues. Cover Image Cover Image. Article Navigation. Conference Article February 01 Carbohydrate metabolism in human adipose tissue in vivo SIMON W. COPPACK ; SIMON W. This Site. Google Scholar. KEITH N. FRAYN ; KEITH N. PATRICIA L. WHYTE ; PATRICIA L. SANDY M. HUMPHREYS SANDY M. Author and article information. Publisher: Portland Press Ltd. Received: June 20 Online ISSN: Biochem Soc Trans 17 1 : — Article history Received:. Get Permissions. toolbar search Search Dropdown Menu. toolbar search search input Search input auto suggest. Article PDF first page preview. Close Modal. You do not currently have access to this content.
Carbohydrate metabolism and lipid storage and breakdown in diabetes	Thus, the pregnant animal appears better poised to mobilize preformed fat whenever exogenous nutrients are withheld. RESERVE YOUR SPOT. In this analysis, we compared lean subjects with NGT with obese subjects with NGT, IGT, and T2DM who were not only more insulin resistant but also more obese on average. By clicking Sign up, I agree to Jack Westin's Terms and Privacy Policy. Sucrose is extracted and purified from sugar cane and sugar beet, while fructose is obtained by the enzymatic degradation of cornstarch into glucose or glucose polymers to be further isomerized enzymatically into fructose, producing the HFCS [ 3 ]. Video Upload Options Do you have a full video?

Carbohydrate metabolism in adipose tissue -

Effects of anoxia, insulin, adrenaline and prolonged starving on concentrations of hexose phosphates in isolated rat diaphragm and perfused isolated rat heart. Manchester : Inhibition of the phosphofructokinase reaction in perfused rat heart by respiration of ketone bodies, fatty acids and pyruvate.

Effects of fatty acids, ketone bodies and pyruvate, and diabetes and starvation, hypophysectomy and adrenalectomy on concentrations of hexose phosphates, nucleotides and inorganic phosphate in perfused isolated rat heart.

Nicholls, D. Garland : Continuous recording techniques for oxygen uptake and carbon dioxide output applied to the study of pyruvate oxidation by rat liver mitochondria.

Orth, D. Morgan : The effect of insulin, alloxan-diabetes, and anoxia on the ultrastructure of the rat heart. Park, C. Morgan, M. Henderson, D. Regen, E. Cadenas and R. Post : The regulation of glucose uptake in muscle as studied in the perfused rat heart.

Recent Progr. Hormone Res. Parmeggiani, A. Bowman : Regulation of phosphofructokinase activity by citrate in normal and diabetic muscle. Passonneau, J. Lowry : Phosphofructokinase and the Pasteur effect. Pearson, O.

Hsieh, C. Du Toit and A. B Hastings : Metabolism of cardiac muscle: utilisation of C 14 labelled pyruvate and acetate in diabetic rat heart. Pogson, C. and P. Randle : The control of rat heart phosphofructokinase by citrate and other regulators. Nature In press b. Randle, P. Garland, C. Hales and E.

Newsholme : The glucose fatty acid cycle. Lancet , I , — Garland : Regulation of glucose uptake by muscle.

Effects of fatty acids, ketone bodies and pyruvate, and diabetes and starvation on uptake and metabolic fate of glucose in rat heart and diaphragm muscles. Newsholme : The glucose fatty acid cycle and Diabetes Mellitus. Denton and C. Pogson : Interactions of metabolism and the physiological role of insulin.

Regen, D. Davies, H. Morgan and C. Park : The regulation of hexokinase and phosphofructokinase activity in heart muscle. Renold, A.

Crofford, W. Stauffacher and B. Jeanrenaud : Hormonal control of adipose tissue metabolism, with special reference to the effects of insulin.

Diabetologia 1 , 4—12 Rizack, M. Scharff, R. Wool : Accumulation of amino acids in muscle of perfused rat heart. Effect of insulin. Shipp, J. Opie and D. Challoner : Fatty acid and glucose metabolism in the perfused rat heart. Thomas and L. Crevasse : Oxidation of C 14 labelled endogenous lipids by isolated perfused rat heart.

Smith, S. Weiss and E. Kennedy : The enzymatic dephosphorylation of phosphatidic acids. Tarrant, M.

Mahler and J. Ashmore : Studies in experimental diabetes. Free fatty acid mobilisation. Villee, C. Hastings : The utilisation in vitro of C 14 labelled acetate and pyruvate by diaphragm muscle of rat.

Visscher, M. Mulder : The carbohydrate metabolism of the heart. Weiss, S. Kennedy : The enzymatic synthesis of triglycerides. Wertheimer, E. Shafrir : Influence of hormones on adipose tissue as a center of fat metabolism. Shapiro : The physiology of adipose tissue.

Wieland, O. Suyter : Glycerokinase: Isolierung und Eigenschaften des Enzyms. Williamson, J. Acetoacetate as fuel of respiration in the perfused rat heart. White, J. Engel : A lipolytic action of epinephrine and norepinephrine on rat adipose tissue in vitro. Download references. Department of Biochemistry, University of Bristol, UK.

You can also search for this author in PubMed Google Scholar. Some of this material also formed the basis for parts of the Banting Memorial Lecture of the British Diabetic Association delivered at the Medical School of the University of Bristol, England, in October, The studies reported have been supported by grants from the British Diabetic Association, the British Insulin Manufacturers, The Medical Research Council, the Science Research Council and the Royal Society.

Reprints and permissions. Carbohydrate metabolism and lipid storage and breakdown in diabetes. Diabetologia 2 , — Download citation. Received : 15 August Issue Date : December Anyone you share the following link with will be able to read this content:.

Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Download PDF. Summary Interactions between the metabolism of glucose and lipids provide the basis for a number of metabolic disturbances which have been observed in clinical and experimental diabetes.

Résumé Les interactions entre le métabolisme du glucose et des lipides fournissent la base d'un certain nombre de troubles métaboliques qui ont été observés dans le diabète clinique et expérimental.

Zusammenfassung Die Zusammenhänge zwischen Glucose- und Fettstoffwechsel sind die Basis für eine Reihe von Stoffwechselstörungen, die beim klinischen und experimentellen Diabetes beobachtet wurden.

Article PDF. Glucose transporters in adipose tissue, liver, and skeletal muscle in metabolic health and disease Article Open access 26 June The muscle protein synthetic response following corn protein ingestion does not differ from milk protein in healthy, young adults Article Open access 05 February Effects of GLP-1 and Its Analogs on Gastric Physiology in Diabetes Mellitus and Obesity Chapter © Use our pre-submission checklist Avoid common mistakes on your manuscript.

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for a euglycemic insulin clamp Catheters were placed in an antecubital vein for the infusion of all test substances and retrogradely into a vein on the dorsum of the hand for blood withdrawal.

The hand was placed in a heated box at 60°C. Plasma glucose concentration was determined by the glucose oxidase method Beckman Glucose Analyzer; Beckman Coulter, Fullerton, CA. Plasma insulin and C-peptide concentrations were measured by radioimmunoassay with specific kits Diagnostic Products Corporation, Los Angeles, CA , and plasma FFA levels were measured spectrophotometrically Wako Chemicals, Neuss, Germany.

Plasma 3- 3 H-glucose levels were measured in Somogyi precipitates as previously described Plasma adiponectin concentration was measured by radioimmunoassay Linco Research, St.

Charles, MO. Insulin sensitivity was assessed by Matsuda index 32 from the plasma glucose and insulin concentrations measured during the OGTT. Insulin resistance was assessed as the inverse of insulin sensitivity. Residual EGP was calculated as R a minus the exogenous glucose infusion rate.

To calculate total body R d , the rate of residual EGP during the last 30 min of the insulin clamp was added to the exogenous glucose infusion rate required to maintain euglycemia during the last 30 min of the insulin clamp. Adipo-IR was calculated as the product of fasting plasma FFA and fasting plasma insulin concentrations and as the product of the mean plasma FFA and insulin concentrations during the OGTT.

Data are mean ± SEM and presented as mean ± SE. Non—normally distributed values were log-transformed before analysis. Group values were compared by ANOVA and Bonferroni-Dunn post hoc analysis.

Univariate associations were tested by Spearman rank correlation. The clinical characteristics of the study subjects are shown in Table 1. Subjects with diabetes were slightly older than those without diabetes but had a similar BMI and percent body fat to obese subjects with NGT and IGT.

In subjects without diabetes NGT and IGT , the FPG concentrations were within the normal range and increased progressively in subjects with T2DM in groups I—III Table 1.

Similarly, the mean plasma glucose concentrations measured during the OGTT increased progressively in T2DM groups I—III Figs. Data are mean ± SE. Subjects with T2DM were grouped according to tertiles of 2h-PG concentrations i. Changes in plasma glucose A , insulin C , and FFA E concentrations during the OGTT in subjects without diabetes.

Changes in plasma glucose B , insulin D , and FFA F concentrations during the OGTT in subjects with T2DM. D, diabetic. Mean plasma glucose A , FFA B , and insulin D concentrations during OGTT; Matsuda index of insulin sensitivity C ; and fasting E and OGTT F Adipo-IR index. G, group; Ins, insulin.

The fasting plasma FFA concentrations were significantly higher in obese NGT and IGT than in lean NGT. The fasting plasma FFA concentration was the lowest in lean NGT, increased markedly and linearly from obese NGT to IGT, and plateaued without further increase in T2DM Table 1.

During the OGTT, the mean plasma FFA concentration was significantly increased in obese NGT versus lean NGT and rose progressively from NGT to IGT Fig. This pattern closely followed the change in Matsuda index of insulin sensitivity and insulin secretion, reflecting the progressive declines in insulin sensitivity Fig.

The fasting plasma insulin concentration progressively increased from NGT to IGT Fig. In marked contrast, the rises in FPG and mean plasma glucose during the OGTT only became pronounced when subjects became overtly diabetic Figs.

Thus, as lean subjects with NGT became obese but still maintained NGT or IGT or T2DM, both the fasting plasma and OGTT FFA as well as glucose concentrations increased Table 1 and Fig. Fasting Adipo-IR increased twofold in obese NGT and IGT versus lean NGT 8. Fasting Adipo-IR was significantly greater in obese T2DM versus lean T2DM This finding was confirmed by analysis of the euglycemic-hyperinsulinemic clamp data Table 1 showing that the plasma FFA concentrations at the end of the hyperinsulinemic clamp were similar in all study groups.

Although fasting Adipo-IR rose continuously in the transition from NGT to IGT to T2DM Fig. Thus, markedly deficient insulin secretion during the OGTT results in a paradoxical decline in OGTT Adipo-IR in T2DM Fig.

We previously have shown that during the transition from NGT to IGT to T2DM, β-cell function progressively declines and peripheral insulin resistance progressively increases 31 , Adipo-IR also is increased in patients with T2DM, but the natural history of its development as individuals progress from NGT to IGT to T2DM has been poorly studied.

As recently reviewed 21 , a number of indices of adipocyte insulin resistance have been proposed that are based on tracer turnover i. In the current study, we used the product of fasting plasma FFA and fasting plasma insulin concentrations as the index of Adipo-IR. Because the circulating plasma FFA concentration closely reflects the rate of peripheral lipolysis, Adipo-IR represents an index for adipose tissue resistance to the antilipolytic effect of insulin.

The hyperbolic relationship between plasma insulin and FFA concentrations initially was demonstrated by Groop et al. Similar results were reported by Bugianesi et al. However, the number of subjects in these previous studies was small, and the changes in Adipo-IR in NGT to IGT to T2DM was not evaluated.

In this cross-sectional study, we evaluated changes in plasma FFA concentration during the fasting state and OGTT in subjects across a wide range of glucose tolerance and insulin resistance.

Subjects with insulin resistance ranging from obese NGT to IGT and T2DM were compared with lean subjects with NGT. The fasting plasma FFA concentration increased markedly and linearly as subjects progressed from lean NGT to obese NGT and IGT and plateaued without further increase in T2DM, reflecting the progressive decline in insulin sensitivity.

The increase in plasma FFA concentration during the OGTT tracks with worsening whole-body insulin resistance and worsening Adipo-IR during the OGTT over the range of NGT to IGT. With progression of IGT to T2DM, the plasma FFA concentration during the OGTT continues to rise, whereas whole-body insulin resistance plateaus and OGTT Adipo-IR declines.

Further progression from NGT to IGT is associated with parallel increases in fasting plasma FFA and worsening whole-body insulin resistance and Adipo-IR.

As IGT progresses to T2DM, no further increase in fasting plasma FFA occurs, even though Adipo-IR continues to worsen. A likely explanation is the observation that the fasting plasma insulin concentration increases sufficiently to offset the worsening of adipocyte insulin resistance.

FFA levels during the OGTT continued to rise in all groups without reaching a plateau as was observed with the fasting plasma FFA concentration primarily because of β-cell dysfunction and reduced insulin secretion in subjects with T2DM, thus following the Starling curve of the pancreas BMI and insulin sensitivity Matsuda index were strongly related to Adipo-IR in both males and females, although Adipo-R was greater in females than in males.

This finding agrees with a previous study by Nielsen et al. The current results, however, are cross-sectional, but they are consistent with those of two prospective studies e.

Therefore, the results of the current analysis show that the fasting Adipo-IR index remains a reliable index of insulin resistance in the fat cell over the entire range of glucose tolerance from NGT to IGT to T2DM.

In contrast, a different picture is observed with Adipo-IR during the OGTT. This dissociation between impaired FFA suppression during the OGTT i. Thus, Adipo-IR during the OGTT does not provide a reliable index of adipocyte insulin resistance in patients with T2DM.

Caution is needed when using the Adipo-IR index in patients with severe fasting hyperglycemia in whom marked insulin deficiency may be present. In contrast to the OGTT, studies with the stepped hyperinsulinemic clamp consistently have demonstrated impaired suppression of plasma FFA and glycerol concentrations and 14 C-palmitate turnover 18 , 22 , 24 i.

The results shown in Figs. These variables are strongly and inversely related. A decrease in β-cell secretion of insulin also is associated with an increase in fasting Adipo-IR.

In this analysis, we compared lean subjects with NGT with obese subjects with NGT, IGT, and T2DM who were not only more insulin resistant but also more obese on average. Subjects with T2DM also were slightly older than those with NGT and IGT. The difference in weight and age could influence FFA levels.

The greater amount of fat in subjects with insulin resistance is likely to contribute to the higher plasma FFA levels.

Older age also influences body composition because older patients usually have more fat than younger patients with the same BMI. However, the effect of aging on insulin action is small, as shown by Ferrannini et al. In summary, the results demonstrate that the fasting adipocyte insulin resistance index fasting FFA × fasting insulin rises progressively over the span of glucose tolerance, ranging from NGT to IGT to T2DM, and provides a valid index of fat cell sensitivity to insulin.

In contrast, the adipocyte insulin resistance index during OGTT rises from NGT to IGT and declines with progression of IGT to T2DM because of the progressive deficiency of insulin secretion in the group with diabetes.

Thus, in the subjects with diabetes, the fasting but not the OGTT adipocyte insulin resistance index provided a reliable measure of fat cell sensitivity to insulin. In conclusion, the progressive decline in β-cell function that begins in individuals with NGT is associated with a progressive increase in FFA and fasting Adipo-IR.

is supported by the Horizon Framework Program of the European Union under Grant Agreement for the project EPoS Elucidating Pathways of Steatohepatitis. Duality of Interest. No potential conflicts of interest relevant to this article were reported.

Author Contributions. and R. contributed to the study design and data analysis and wrote the manuscript. contributed to the data analysis, discussion, and writing of the manuscript.

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Interactions Cagbohydrate the metabolism Natural metabolism-boosting drinks glucose and un provide the basis for a number of metabolic disturbances which have been Leafy greens for glowing skin tiesue clinical and experimental diabetes. Particular metaabolism Leafy greens for glowing skin meyabolism which may be Carbohydrate metabolism in adipose tissue in the storage mstabolism mobilisation of aeipose and Leafy greens for glowing skin the relative contribution of glucose afipose fatty acid to energy needs. The concept of a Glucose Fatty Acid Cycle is reviewed and forms the basis for recent studies which are outlined. An essential feature of the Cycle is the proposal that the normal relationship between glucose and fatty acid metabolism is reciprocal and not dependent; and that the augmented release of fatty acids for oxidation in muscle and other tissues in diabetes is not primarily due to defective glucose metabolism. The release and oxidation of fatty acids may depend upon lipolysis which may be directly regulated by hormone action and not dependent upon glucose metabolism. It can also depend upon esterification of fatty acids which may involve the metabolism of glucose to glycerol phosphate. Evidence is presented that lipid mobilization in the alloxan-diabetic rat which may be insensitive to inhibition by insulin action is primarily dependent upon activation of lipolysis. SIMON W. COPPACK,etabolism N. FRAYNPATRICIA L. WHYTESANDY M. HUMPHREYS; Carbohydrate metabolism in human adipose tissue in vivo. Biochem Soc Trans 1 February ; 17 1 : — Sign In or Create an Account.