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Exercise Has Been Shown To Enhance Insulin Action In Skeletal Muscle

Potential Role Of Tbc1d4 In Enhanced Post-exercise Insulin Action In Human Skeletal Muscle

Potential Role Of Tbc1d4 In Enhanced Post-exercise Insulin Action In Human Skeletal Muscle

, Volume 52, Issue5 , pp 891900 | Cite as Potential role of TBC1D4 in enhanced post-exercise insulin action in human skeletal muscle TBC1 domain family, member 4 (TBC1D4; also known as AS160) is a cellular signalling intermediate to glucose transport regulated by insulin-dependent and -independent mechanisms. Skeletal muscle insulin sensitivity is increased after acute exercise by an unknown mechanism that does not involve modulation at proximal insulin signalling intermediates. We hypothesised that signalling through TBC1D4 is involved in this effect of exercise as it is a common signalling element for insulin and exercise. Insulin-regulated glucose metabolism was evaluated in 12 healthy moderately trained young men 4h after one-legged exercise at basal and during a euglycaemichyperinsulinaemic clamp. Vastus lateralis biopsies were taken before and immediately after the clamp. Insulin stimulation increased glucose uptake in both legs, with greater effects (~80%, p < 0.01) in the previously exercised leg. TBC1D4 phosphorylation, assessed using the phosphoAKT (protein kinase B)substrate antibody and phospho- and site-specific antibodies targeting six phosphorylation sites on TBC1D4, increased at similar degrees to insulin stimulation in the previously exercised and rested legs (p < 0.01). However, TBC1D4 phosphorylation on Ser-318, Ser-341, Ser-588 and Ser-751 was higher in the previously exercised leg, both in the absence and in the presence of insulin (p < 0.01; Ser-588, p = 0.09; observed power = 0.39). 1433 binding capacity for TBC1D4 increased equally (p < 0.01) in both legs during insulin stimulation. We provide evidence for site-specific phosphorylation of TBC1D4 in human skeletal muscle in response to physiological hyperinsulinaemia. The data support the idea th Continue reading >>

Diabetes, Mitochondria And Exercise

Diabetes, Mitochondria And Exercise

Rev Esp Cardiol. 2008;8(Supl C):25-32 - Vol. 8 Num.Supl.C Katja SC Rckl a, Carol A Witczak a, Laurie J Goodyear a a Research Division. Joslin Diabetes Center and Department of Medicine. Brigham and Women's Hospital and Harvard Medical School. Harvard. MA. USA. Skeletal muscle. Glucose transport. Fibre type. Exercise has beneficial effects on overall health, and its role in the treatment and prevention of insulin resistance and type 2 diabetes is undisputed. An acute bout of exercise or muscle contraction increases glucose uptake into skeletal muscle through insulin independent pathways, which leads to improvements in whole body glucose homeostasis. Regular physical activity induces adaptative changes in skeletal muscle through modification of metabolic gene expression. Such changes include increases in mitochondria and alteration of muscle fiber type distribution. An important goal of exercise research is to study molecular signals that are induced by muscle activity and that regulate key metabolic and transcriptional events in skeletal muscle. In this review, we give a brief overview of exercise research in the metabolic field, describing a number of molecular signals underlying these events. In this dynamic field of research the search for additional exercise-stimulated signalling proteins is ongoing. Studies to further elucidate exercise-mediated pathways involved in glucose transport, muscle fibre type and mitochondrial biogenesis will help to further understand the beneficial effects of exercise, to improve our knowledge about the pathological mechanisms of metabolic diseases such as type 2 diabetes, and to find new pharmacological targets for treatment. Throughout the world, diabetes currently afflicts over 180 million people, and epidemiological estimates from t Continue reading >>

Ampk Is Required For Exercise To Enhance Insulin Sensitivity In Skeletal Muscles

Ampk Is Required For Exercise To Enhance Insulin Sensitivity In Skeletal Muscles

The signaling mechanisms by which exercise improves muscle insulin sensitivity seem even harder to solve than to get people to exercise. Exercise (muscle contraction) has two diverse effects on muscle glucose metabolism. Firstly, acute exercise stimulates glucose uptake in skeletal muscles via translocation of GLUT4 translocation. This effect is insulin independent, and glucose uptake remains elevated a couple of hours after termination of exercise. Secondly, exercise increases insulin sensitivity in skeletal muscles. This latter effect remains for many hours after cessation of exercise, and is obviously insulin dependent. Indeed, candidates have been abundant for both effects of exercise, but convincing signalling mechanisms have not emerged [1]. From a health perspective, the improved muscle insulin sensitivity in the period after exercise improves metabolic regulation. The observation that muscle contraction increases insulin action in prior active muscle was reported in 1982 by Richter et al. [2]. Until now, the most important finding on the mechanisms governing insulin action after exercise is the reports from Holloszy's laboratory in the 1980s describing that the glycogen content in muscles determines insulin sensitivity after exercise. These studies showed that carbohydrate feeding reduced insulin sensitivity in muscles, whereas insulin sensitivity remained elevated when muscle glycogen content was kept low [[3], [4]]. Indeed, glycogen has kept its central position in regulation of insulin action and capacity to store glucose in muscles [[5], [6]], but little progress has occurred on the mechanisms for elevated muscle insulin sensitivity after exercise. It was obvious to look for enhanced activation of the insulin signaling pathway, but this research has been dis Continue reading >>

Modulation Of Insulin Signaling In Human Skeletal Muscle In Response To Exercise

Modulation Of Insulin Signaling In Human Skeletal Muscle In Response To Exercise

Obesity has become a health problem of epidemic proportions in the United States during the last several decades, with approximately one quarter of the population classified as obese. Over 80% of these individuals have some form of insulin resistance and it is estimated that 16 million people (6% of the total population) suffer from diabetes. Of those, over 90% are classified as having type II diabetes mellitus (DM), which is characterized by defects in both insulin action on its target tissues (skeletal muscle, adipose, and liver), and insulin secretion from the pancreas. It has become increasingly clear that the development of obesity and type II DM is influenced by the interaction of both genetic and environmental factors. Most models describing type II DM suggest that the disease develops in genetically susceptible individuals whose lifestyles feature low levels of physical activity and a high-calorie, high-fat diet. One of the key pathogenic features of type II DM is a resistance to the stimulatory effect of insulin on glucose transport and use in skeletal muscle, which is the main site of postprandial glucose disposal. Currently it is thought that the primary defect causing insulin resistance in skeletal muscle is at the level of insulin-stimulated glucose transport, rather than glucose phosphorylation and use. Thus, a molecular defect distal to the insulin receptor is a primary candidate in explaining the defect that leads to abnormal metabolism in type II DM. Such a molecular mechanism may include decreased expression and/or activation of key intracellular proteins that orchestrate the signal from insulin to its target glucose transporter, which is glucose transport isoform 4 (GLUT4) in skeletal muscle. If this were the case, a treatment targeted toward the reg Continue reading >>

Insulin Resistance And Skeletal Muscle Vasculature: Significance, Assessment And Therapeutic Modulators

Insulin Resistance And Skeletal Muscle Vasculature: Significance, Assessment And Therapeutic Modulators

Insulin Resistance and Skeletal Muscle Vasculature: Significance, Assessment and Therapeutic Modulators Division of Endocrinology, Department of Internal Medicine, University of Missouri D109 Diabetes Center HSC, 1 Hospital Drive Overnutrition and sedentarism are closely related to the alarming incidence of obesity and type 2 diabetes mellitus (DM2) in the Western world. Resistance to the actions of insulin is a common occurrence in conditions such as obesity, hypertension and DM2. In the skeletal muscle vasculature, insulin promotes vasodilation and its own transport across the vascular wall to reach its target tissue. Furthermore, insulin resistance (IR) in the skeletal muscle vasculature results in impaired skeletal muscle glucose uptake and altered whole-body glucose homeostasis. The development of different invasive and noninvasive techniques has allowed the characterization of the actions of insulin and other vasoactive hormones in the skeletal muscle vasculature in both health and disease. Current treatment strategies for DM2 do not necessarily address the impaired effect of insulin in the vasculature. Understanding the effects of insulin and other metabolically active hormones in the vasculature should facilitate the development of new therapeutic strategies targeted at the modulation of IR and improvement of whole-body glucose tolerance. i 2014 S. Karger AG, Basel The impact of type 2 diabetes mellitus (DM2) continues to grow, affecting 26 million individuals in the United States and 347 million worldwide [ 1 ]. Resistance to the metabolic actions of insulin is an important contributor to the pathogenesis of DM2 [ 2 ], and, despite the availability of different pharmacological strategies for the treatment of DM2, the options available to diminish insulin resis Continue reading >>

Pathogenesis Of Insulin Resistance In Skeletal Muscle

Pathogenesis Of Insulin Resistance In Skeletal Muscle

Journal of Biomedicine and Biotechnology Volume 2010 (2010), Article ID 476279, 19 pages Division of Diabetes, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr, San Antonio, TX 78229, USA Academic Editor: Guy M. Benian Copyright © 2010 Muhammad A. Abdul-Ghani and Ralph A. DeFronzo. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Insulin resistance in skeletal muscle is manifested by decreased insulin-stimulated glucose uptake and results from impaired insulin signaling and multiple post-receptor intracellular defects including impaired glucose transport, glucose phosphorylation, and reduced glucose oxidation and glycogen synthesis. Insulin resistance is a core defect in type 2 diabetes, it is also associated with obesity and the metabolic syndrome. Dysregulation of fatty acid metabolism plays a pivotal role in the pathogenesis of insulin resistance in skeletal muscle. Recent studies have reported a mitochondrial defect in oxidative phosphorylation in skeletal muscle in variety of insulin resistant states. In this review, we summarize the cellular and molecular defects that contribute to the development of insulin resistance in skeletal muscle. 1. Introduction Skeletal muscle is the major site for disposal of ingested glucose in lean healthy normal glucose tolerance (NGT) individuals [1–4]. Following a meal, approximately one third of ingested glucose is taken up by the liver and the rest by peripheral tissues, primarily skeletal muscle via an insulin dependent mechanism [1–4]. The postprandial hyperglycemia stimulates insulin secretion from the pancreas and the Continue reading >>

Glucose, Exercise And Insulin: Emerging Concepts

Glucose, Exercise And Insulin: Emerging Concepts

Glucose, exercise and insulin: emerging concepts Erik A Richter , Wim Derave ,* and Jrgen F P Wojtaszewski *Laboratory of Exercise Physiology and Biomechanics, Faculty of Physical Education and Physiotherapy, Katholieke Universiteit Leuven, B-3001 Leuven, Belgium Copenhagen Muscle Research Centre, Department of Human Physiology, Institute of Exercise and Sports Sciences, University of Copenhagen, DK-2100 Copenhagen, Denmark *Laboratory of Exercise Physiology and Biomechanics, Faculty of Physical Education and Physiotherapy, Katholieke Universiteit Leuven, B-3001 Leuven, Belgium Corresponding author E. A. Richter: Copenhagen Muscle Research Centre, Institute of Exercise and Sports Sciences, University of Copenhagen, 13 Universitetsparken, DK-2100 Copenhagen, Denmark. Email: [email protected] Received 2001 May 30; Accepted 2001 Jul 13. Copyright The Physiological Society 2001 This article has been cited by other articles in PMC. Physical exercise induces a rapid increase in the rate of glucose uptake in the contracting skeletal muscles. The enhanced membrane glucose transport capacity is caused by a recruitment of glucose transporters (GLUT4) to the sarcolemma and t-tubules. This review summarises the recent progress in the understanding of signals that trigger GLUT4 translocation in contracting muscle. The possible involvement of calcium, protein kinase C (PKC), nitric oxide (NO), glycogen and AMP-activated protein kinase (AMPK) are discussed. Furthermore, the possible mechanisms behind the well-described improvement of insulin action on glucose uptake and glycogen synthase activity in the post-exercise period is discussed. It is concluded that both during and following muscle contractions, glycogen emerges as an important modulator of signalling events in glucose meta Continue reading >>

The Role Of Skeletal Muscle Glycogen Breakdown For Regulation Of Insulin Sensitivity By Exercise

The Role Of Skeletal Muscle Glycogen Breakdown For Regulation Of Insulin Sensitivity By Exercise

1 Department of Physical Performance, Norwegian School of Sport Sciences, Oslo, Norway 2 Third Faculty of Medicine, Department of Medicine, Charles University, Prague, Czech Republic 3 Protein Phosphorylation Research Group, de Duve Institute, Université Catholique de Louvain, Brussels, Belgium Glycogen is the storage form of carbohydrates in mammals. In humans the majority of glycogen is stored in skeletal muscles (∼500 g) and the liver (∼100 g). Food is supplied in larger meals, but the blood glucose concentration has to be kept within narrow limits to survive and stay healthy. Therefore, the body has to cope with periods of excess carbohydrates and periods without supplementation. Healthy persons remove blood glucose rapidly when glucose is in excess, but insulin-stimulated glucose disposal is reduced in insulin resistant and type 2 diabetic subjects. During a hyperinsulinemic euglycemic clamp, 70–90% of glucose disposal will be stored as muscle glycogen in healthy subjects. The glycogen stores in skeletal muscles are limited because an efficient feedback-mediated inhibition of glycogen synthase prevents accumulation. De novo lipid synthesis can contribute to glucose disposal when glycogen stores are filled. Exercise physiologists normally consider glycogen’s main function as energy substrate. Glycogen is the main energy substrate during exercise intensity above 70% of maximal oxygen uptake () and fatigue develops when the glycogen stores are depleted in the active muscles. After exercise, the rate of glycogen synthesis is increased to replete glycogen stores, and blood glucose is the substrate. Indeed insulin-stimulated glucose uptake and glycogen synthesis is elevated after exercise, which, from an evolutional point of view, will favor glycogen repletion a Continue reading >>

Exercise Training-induced Improvements In Insulin Action.

Exercise Training-induced Improvements In Insulin Action.

1. Acta Physiol (Oxf). 2008 Jan;192(1):127-35. doi:10.1111/j.1748-1716.2007.01783.x. Exercise training-induced improvements in insulin action. (1)Exercise Metabolism Group, School of Medical Sciences, RMIT University, Bundoora, Vic., Australia. [email protected] Individuals with insulin resistance are characterized by impaired insulin action on whole-body glucose uptake, in part due to impaired insulin-stimulated glucose uptake into skeletal muscle. A single bout of exercise increases skeletal muscle glucose uptake via an insulin-independent mechanism that bypasses the typicalinsulin signalling defects associated with these conditions. However, this'insulin sensitizing' effect is short-lived and disappears after approximately 48h. In contrast, repeated physical activity (i.e. exercise training) results in a persistent increase in insulin action in skeletal muscle from obese andinsulin-resistant individuals. The molecular mechanism(s) for the enhancedglucose uptake with exercise training have been attributed to the increasedexpression and/or activity of key signalling proteins involved in the regulation of glucose uptake and metabolism in skeletal muscle. Evidence now suggests thatthe improvements in insulin sensitivity associated with exercise training arealso related to changes in the expression and/or activity of proteins involved ininsulin signal transduction in skeletal muscle such as the AMP-activated protein kinase (AMPK) and the protein kinase B (Akt) substrate AS160. In addition,increased lipid oxidation and/or turnover is likely to be another mechanism bywhich exercise improves insulin sensitivity: exercise training results in anincrease in the oxidative capacity of skeletal muscle by up-regulating lipidoxidation and the expression of proteins involved i Continue reading >>

Direct Cross-talk Of Interleukin-6 And Insulin Signal Transduction Via Insulin Receptor Substrate-1 In Skeletal Muscle Cells*

Direct Cross-talk Of Interleukin-6 And Insulin Signal Transduction Via Insulin Receptor Substrate-1 In Skeletal Muscle Cells*

The exercise-induced interleukin (IL)-6 production and secretion within skeletal muscle fibers has raised the question of a putative tissue-specific function of IL-6 in the energy metabolism of the muscle during and after the exercise. In the present study, we followed the hypothesis that IL-6 signaling may directly interact with insulin receptor substrate (IRS)-1, a keystone in the insulin signaling cascade. We showed that IL-6 induces a rapid recruitment of IRS-1 to the IL-6 receptor complex in cultured skeletal muscle cells. Moreover, IL-6 induced a rapid and transient phosphorylation of Ser-318 of IRS-1 in muscle cells and in muscle tissue, but not in the liver of IL-6-treated mice, probably via the IL-6-induced co-recruitment of protein kinase C-. This Ser-318 phosphorylation improved insulin-stimulated Akt phosphorylation and glucose uptake in myotubes since transfection with an IRS-1/Glu-318 mutant simulating a permanent phospho-Ser-318 modification increased Akt phosphorylation and glucose uptake. Noteworthily, two inhibitory mechanisms of IL-6 on insulin action, phosphorylation of the inhibitory Ser-307 residue of IRS-1 and induction of SOCS-3 expression, were only found in liver but not in muscle of IL-6-treated mice. Thus, the data provided evidence for a possible molecular mechanism of the physiological metabolic effects of IL-6 in skeletal muscle, thereby exerting short term beneficial effects on insulin action. Over the last two decades, the pleiotropic cytokine interleukin-6 (IL-6) 2 has been looked upon as a major component in the inflammatory network and the acute immune response ( 1 ). Since 1997, when the adipose tissue was recognized as a relevant IL-6 producing organ, accounting for 1035% of circulating IL-6 plasma levels in humans ( 2 ), this view Continue reading >>

Skeletal Muscle Glucose Uptake Following Overload-induced Hypertrophy

Skeletal Muscle Glucose Uptake Following Overload-induced Hypertrophy

Skeletal muscle glucose uptake following overload-induced hypertrophy Author links open overlay panel J.C.Young Get rights and content While endurance exercise training has been shown to enhance insulin action in skeletal muscle, the effects of high resistance strength training are less clear. The purpose of this study was to determine the rate of glucose uptake in skeletal muscle in which compensatory hypertrophy was induced by synergist muscle ablation. Basal and insulin mediated [3H] 2-deoxyglucose uptake were measured in soleus and EDL muscles using the perfused rat hindquarter preparation. Neither basal nor insulin mediated glucose uptake, when expressed per gram muscle, were enhanced in hypertrophied soleus muscles compared with control muscles, despite a twofold increase in mass (P < 0.01). In the EDL, muscle mass increased 60% with synergist ablation (P < 0.01), however insulin mediated glucose uptake was not different from that of control muscles. The basal rate of glucose uptake in hypertrophied EDL muscles was increased twofold over that of control muscles (P < 0.05), possibly due to changes in neural input and/or loading. These results suggest that the stimulus for development of increased muscle mass is different from that for metabolic adaptations. Continue reading >>

Skeletal Muscle Insulin Resistance: Roles Of Fatty Acid Metabolism And Exercise

Skeletal Muscle Insulin Resistance: Roles Of Fatty Acid Metabolism And Exercise

Skeletal Muscle Insulin Resistance: Roles of Fatty Acid Metabolism and Exercise LP Turcotte, PhD, is Associate Professor and Chair, Department of Kinesiology, University of Southern California, Los Angeles, California. JS Fisher, PhD, is Associate Professor, Department of Biology, Saint Louis University, 3507 Laclede Ave, St Louis, MO 63103 (USA). LP Turcotte, PhD, is Associate Professor and Chair, Department of Kinesiology, University of Southern California, Los Angeles, California. JS Fisher, PhD, is Associate Professor, Department of Biology, Saint Louis University, 3507 Laclede Ave, St Louis, MO 63103 (USA). Address all correspondence to Dr Fisher at: [email protected] Received 2008 Jan 15; Accepted 2008 May 8. Copyright 2008, American Physical Therapy Association This article has been cited by other articles in PMC. The purpose of this review is to provide information about the role of exercise in the prevention of skeletal muscle insulin resistance, that is, the inability of insulin to properly cause glucose uptake into skeletal muscle. Insulin resistance is associated with high levels of stored lipids in skeletal muscle cells. Aerobic exercise training decreases the amounts of these lipid products and increases the lipid oxidative capacity of muscle cells. Thus, aerobic exercise training may prevent insulin resistance by correcting a mismatch between fatty acid uptake and fatty acid oxidation in skeletal muscle. Additionally, a single session of aerobic exercise increases glucose uptake by muscle during exercise, increases the ability of insulin to promote glucose uptake, and increases glycogen accumulation after exercise, all of which are important to blood glucose control. There also is some indication that resistance exercise may be effective in preventing ins Continue reading >>

Enhanced Insulin Sensitivity In Successful, Long-term Weight Loss Maintainers Compared With Matched Controls With No Weight Loss History

Enhanced Insulin Sensitivity In Successful, Long-term Weight Loss Maintainers Compared With Matched Controls With No Weight Loss History

Original Article | Open Enhanced insulin sensitivity in successful, long-term weight loss maintainers compared with matched controls with no weight loss history Nutrition & Diabetes volume 7, page e282 (2017) Weight gain is associated with deterioration in metabolic health, whereas weight loss improves insulin sensitivity. This study assesses the impact of long-term, successfully maintained weight loss and weight-loss relapse on measures of insulin sensitivity and identifies factors that explain variability in insulin sensitivity. Women (2045 years) were recruited into four groups: reduced-overweight/obese (RED, n=15); body mass index (BMI)-matched controls (stable low-weight, n=19), BMI27 kg m2; relapsed-overweight/obese subjects (REL, n=11); and BMI-matched controls (obese stable weight, n=11), BMI27 kg m2. A 75 g oral glucose tolerance test determined fasting and 2 h plasma glucose and insulin. Homeostatic Model Assessment (HOMA-IR) and insulin sensitivity index (ISI(0,120)) assessed insulin sensitivity. Anthropometric measurements, fasting resting metabolic rate (RMR) and respiratory quotient (RQ) were measured. Questionnaires and dietary intake were recorded, and physical activity was measured using accelerometers. RED were more insulin sensitive, characterised by lower fasting (P=0.001) and 2 h insulin (P=0.003) levels compared with all other groups. There were no significant differences in dietary intake, sedentary, light and moderate activity, RMR or RQ in the RED compared with the other three groups. % Body weight (BW) lost (P<0.001), % BW regained (P<0.05), body fat %, light activity (P<0.05, only log HOMA), vigorous activity (P<0.05) and RQ (P<0.01) predicted 61.4% and 59.7% of variability in log HOMA and log ISI(0,120), respectively, in multiple linear regr Continue reading >>

Exercise And Insulin Sensitivity: A Review.

Exercise And Insulin Sensitivity: A Review.

Abstract Physical activity has a beneficial effect on insulin sensitivity in normal as well as insulin resistant populations. A distinction should be made between the acute effects of exercise and genuine training effects. Up to two hours after exercise, glucose uptake is in part elevated due to insulin independent mechanisms, probably involving a contraction-induced increase in the amount of GLUT4 associated with the plasma membrane and T-tubules. However, a single bout of exercise can increase insulin sensitivity for at least 16 h post exercise in healthy as well as NIDDM subjects. Recent studies have accordingly shown that acute exercise also enhances insulin stimulated GLUT4 translocation. Increases in muscle GLUT4 protein content contribute to this effect, and in addition it has been hypothesized that the depletion of muscle glycogen stores with exercise plays a role herein. Physical training potentiates the effect of exercise on insulin sensitivity through multiple adaptations in glucose transport and metabolism. In addition, training may elicit favourable changes in lipid metabolism and can bring about improvements in the regulation of hepatic glucose output, which is especially relevant to NIDDM. It is concluded that physical training can be considered to play an important, if not essential role in the treatment and prevention of insulin insensitivity. Continue reading >>

Effects Of Exercise Training On Regulation Of Skeletal Muscle Glucose Metabolism In Elderly Men

Effects Of Exercise Training On Regulation Of Skeletal Muscle Glucose Metabolism In Elderly Men

Effects of Exercise Training on Regulation of Skeletal Muscle Glucose Metabolism in Elderly Men Department of Nutrition, Exercise and Sports, University of Copenhagen Department of Nutrition, Exercise and Sports, University of Copenhagen Department of Nutrition, Exercise and Sports, University of Copenhagen Department of Nutrition, Exercise and Sports, University of Copenhagen The Journals of Gerontology: Series A, Volume 70, Issue 7, 1 July 2015, Pages 866872, Rasmus Sjrup Biens, Jesper Olesen, Lasse Gliemann, Jakob Friis Schmidt, Mikkel Sillesen Matzen, Jrgen F. P. Wojtaszewski, Ylva Hellsten, Henriette Pilegaard; Effects of Exercise Training on Regulation of Skeletal Muscle Glucose Metabolism in Elderly Men, The Journals of Gerontology: Series A, Volume 70, Issue 7, 1 July 2015, Pages 866872, The aim was to investigate the molecular mechanisms behind exercise training-induced improvements in glucose regulation in aged subjects. Twelve elderly male subjects completed 8 weeks of exercise training. Before and after the training period, the subjects completed an oral glucose tolerance test (OGTT) and a muscle biopsy was obtained from the vastus lateralis before and 45 minutes into the OGTT. Blood samples were collected before and up to 120 minutes after glucose intake. Exercise training increased Hexokinase II, GLUT4, Akt2, glycogen synthase (GS), pyruvate dehydrogenase (PDH)-E1, PDK2 protein, and glycogen content in skeletal muscle. Furthermore, in response to glucose, GS activity was increased and the dephosphorylation of GS site 2 + 2a and 3a was enhanced after the training intervention. The glucose-mediated insulin stimulation of TBC1D4 Thr642 phosphorylation was increased after exercise training. In the trained state, the PDHa activity was reduced following glucose Continue reading >>

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