Download or read book Skeletal Muscle Glucose Transport Following Exercise in Rodents written by Charles L. Dumke and published by . This book was released on 2000 with total page 266 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book Persistent Effects of Exercise of Skeletal Muscle Glucose Transport Across a Portion of the Life span of F344XBNNia Rats written by Carol A. Briggs-Tung and published by . This book was released on 1993 with total page 118 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book Post exercise Insulin Sensitivity in Rodent Skeletal Muscle written by Junghoon Kim and published by . This book was released on 2005 with total page 202 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book Characterization of the Glucose Transporters Responsible for Mechanical Overloadstimulated Glucose Uptake in Mouse Skeletal Muscle written by Shawna McMillin and published by . This book was released on 2020 with total page 108 pages. Available in PDF, EPUB and Kindle. Book excerpt: Resistance exercise training is a recommended form of physical activity for people with type 2 diabetes due to its ability to increase skeletal muscle glucose uptake. Understanding how resistance training controls muscle glucose uptake may lead to new type 2 diabetes treatments. Therefore, the overall objective of this dissertation was to identity the glucose transporter(s) that mediate muscle glucose uptake in response to mechanical overload, a model of resistance exercise training in rodents. Aim 1: Determine if glucose transporter 4 (GLUT4) is necessary for \ overload-stimulated skeletal muscle glucose uptake. Overload was induced by unilateral synergist ablation in the plantaris muscles of muscle-specific GLUT4 knockout mice. After 5 days, muscle glucose uptake was assessed. Intriguingly, the loss of GLUT4 did not impair the ability of overload to stimulate muscle glucose uptake. This exciting finding demonstrated that resistance training/mechanical overload stimulates muscle glucose uptake via a novel, exercise-responsive glucose transporter. Additional key characteristics of this novel transporter were identified and included: 1) localization to the plasma membrane; 2) ability to transport D-glucose, 2-deoxy-D-glucose, D-galactose and D xylose, but not D-fructose; and 3) binds the chemical cytochalasin B. Aim 2: Determine if glucose transporter 1 (GLUT1) is necessary for overload-stimulated skeletal muscle glucose uptake. Overload was induced by unilateral synergist ablation in the plantaris muscles of muscle-specific GLUT1 knockout mice. After 5 days, muscle glucose uptake was assessed. Surprisingly, the loss of GLUT1 did not impair either basal or overload-stimulated muscle glucose uptake. These unexpected findings demonstrated that the role of GLUT1 in muscle is presently unknown. In addition, this aim identified another key characteristic of the novel exercise/mechanical overload-responsive glucose transporter. The characteristic is that it binds the chemical BAY-876. These findings are significant because they challenge the dogma that in skeletal muscle that GLUT1 is the sole regulator of glucose uptake in the basal state and that GLUT4 is the sole exercise-responsive glucose transporter. In addition, this research represents a critical first step in the development of new type 2 diabetes therapies designed to utilize similar mechanisms as resistance training to stimulate glucose uptake into muscle.
Download or read book Skeletal Muscle Metabolism in Exercise and Diabetes written by Erik A. Richter and published by Springer Science & Business Media. This book was released on 2013-11-11 with total page 325 pages. Available in PDF, EPUB and Kindle. Book excerpt: The Copenhagen Muscle Research Centre was founded in 1994 with the support of a grant from the Danish National Research Foundation. Among the goals for the Centre is the organization of research symposia, with the aim of bringing a limited number ofintemation ally renowned scientists together to discuss the latest developments and perspectives in their field. The first Copenhagen Muscle Research Centre Conference was held in 1995 and dealt with cardiovascular regulation. The Second Copenhagen Muscle Research Centre Confer ence was held from October 23-26, 1997. The topic of the Symposium was Muscle Metabo lism: Regulation, Exercise, and Diabetes. Seventy invited scientists from all over the world discussed their latest research related to skeletal muscle metabolism. The speakers were asked to expand on their presentations and to write short, but comprehensive, chapters about their given topics. The result is 28 peer-reviewed and edited chapters covering many if not all aspects of muscle energy metabolism related to exercise and diabetes. Emphasis is on regulation of glucose and fatty acid metabolism and the mechanisms regulating their use as fuels for the muscle during exercise. In addition, abnormalities in the regulation of glucose metabolism in the diabetic state are described. However, amino acid and protein metabolism are also thoroughly discussed. We believe that this volume brings an unparralleled, up to date, and comprehensive review of the frontiers in muscle metabolism. Erik A.
Download or read book Influence of Calorie Restriction on Insulin Signalling and Glucose Transport in Skeletal Muscle of Rats written by David J. Dean and published by . This book was released on 1997 with total page 512 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book Glucose Transport Into Skeletal Muscle written by Harriet Wallberg-Henriksson and published by . This book was released on 1987 with total page 92 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book Skeletal Muscle Insulin Receptor Function and Glucose Uptake in Aging Rats written by Kristin Carlson Eiffert and published by . This book was released on 1991 with total page 248 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book Effects of Exercise Training on the Glucose Transport System in Isolated Rat Skeletal Muscle written by Thomas Henry Reynolds and published by . This book was released on 1996 with total page 258 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book Effects of Acute Exercise on Sarcolemmal Glucose Transport and Plasma Glucose in Streptozotocin induced Diabetic Rats with Normal and Altered GLUT 4 Expression written by Lisa Dianne Hackney and published by . This book was released on 1993 with total page 88 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book Glucose transport in exercising and non exercising skeletal muscle after exercise written by Lynn A. Megeney and published by . This book was released on 1991 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book Hormones Metabolism and the Benefits of Exercise written by Bruce Spiegelman and published by Springer. This book was released on 2018-03-07 with total page 108 pages. Available in PDF, EPUB and Kindle. Book excerpt: The world is faced with an epidemic of metabolic diseases such as obesity and type 2 diabetes. This is due to changes in dietary habits and the decrease in physical activity. Exercise is usually part of the prescription, the first line of defense, to prevent or treat metabolic disorders. However, we are still learning how and why exercise provides metabolic benefits in human health. This open access volume focuses on the cellular and molecular pathways that link exercise, muscle biology, hormones and metabolism. This will include novel “myokines” that might act as new therapeutic agents in the future.
Download or read book Insulin Action written by Ashok K. Srivastava and published by Springer Science & Business Media. This book was released on 1998-05-31 with total page 206 pages. Available in PDF, EPUB and Kindle. Book excerpt: In 1996 the 75th anniversary of the discovery of insulin was celebrated at the University of Toronto, the scene of that discovery in 1921. This volume was stimulated by the scientific program which was staged at that time and brought together much of the world's best talent to discuss and analyze the most recent developments in our understanding of pancreatic function, insulin secretion, the interaction of insulin with its target tissues, the mechanism of insulin action at the cellular level, and the defects which underlie both Type I (insulin-dependent diabetes mellitus, IDDM) and Type II (noninsulin-dependent diabetes mellitus, NIDDM) forms of the disease. We have chosen to focus the present volume on work related to insulin action.
Download or read book Mechanisms of Exercise and Insulin Action on Glucose Transport in Rat Skeletal Muscle Sarcolemmal Vesicles written by Eric Sternlicht and published by . This book was released on 1987 with total page 170 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Download or read book The Relationship Between Elevations in Glucocorticoids and Diabetes Development in Rats on Skeletal Muscle Insulin Resistance and the Microvasculature written by Emily Dunford and published by . This book was released on 2016 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: Elevations in GC concentrations are well-known to cause a variety of negative systemic side effects, and subtle alterations in GC secretion and tissue-specific actions are a possible link between insulin resistance, the metabolic syndrome and T2DM development. These pathological conditions impair insulin-stimulated skeletal muscle blood flow and glucose uptake, in addition to causing profound myopathy, all of which could be significant contributors to the metabolic complications associated with insulin resistance. The focus of this dissertation was to understand how elevations in GC concentrations can be associated with skeletal muscle insulin resistance and diabetes development and whether augmentation to the muscle microvasculature is beneficial or even possible during conditions that generate significant exposure to elevations in GCs. To examine these situations, two rodent models of diabetes were used; exogenous elevations in GCs either combined with a HFD or provided a standard chow diet, to reproduce T2DM, and STZ-treated rats to induce -cell destruction, simulating T1DM. As both regular exercise and circulating insulin levels have been well documented in the regulation of microvascular augmentation, we assessed the therapeutic potential of voluntary exercise and pharmacologically enhancing hyperemia in both GC-induced skeletal muscle insulin resistance and STZ-induced diabetes. We revealed that the skeletal muscle is severely altered (decreased glycolytic muscle insulin-stimulated glucose transport and considerable glycolytic fibre atrophy) in the presence of hypercortisolemia coupled with HFD, but these alterations could be attenuated with the administration of voluntary aerobic exercise. The hypercortisolemia also resulted in alterations to the microvasculature (capillary rarefaction), which, when attenuated through 1-antagonism, produced a correlative enhancement in insulin sensitivity. Finally, the combination of voluntary exercise and 1-antagonism, in a model of chemically-induced (STZ) diabetes, demonstrated synergistic qualities through the increase in capillary growth within both glycolytic and oxidative skeletal muscle and enhanced glycemic control. This thesis provides considerable evidence proving that manipulation of the skeletal muscle microvasculature, either through voluntary exercise or pharmacologically enhanced hyperemia, can attenuate the hypercortisolemia-induced skeletal muscle capillary rarefaction and improve glucose metabolism through enhanced glucose uptake and insulin sensitivity.
Download or read book Effects of Exercise Training on Skeletal Muscle Insulin Signaling and Inflammation in Two Rodent Models of Insulin Resistance written by Lindsea Burns and published by . This book was released on 2016 with total page 48 pages. Available in PDF, EPUB and Kindle. Book excerpt: The aims of this investigation were 1) to determine if resistance exercise training, like aerobic exercise training, improves insulin signaling in the skeletal muscle of the high fat-fed Sprague Dawley rat via suppression of the IKK inflammatory pathway, and 2) to determine if aerobic and resistance training are equally effective at improving skeletal muscle insulin resistance in the obese Zucker rat, and if these improvements are due to suppression of the IKK inflammatory pathway. Sprague Dawley rats were placed on a chow (NC, n=8) or high-fat (n=24) diet, while the Zucker rats (n=32) were fed a normal chow diet, for 4wks. During the subsequent 8-wk experimental protocol, high fat-fed Sprague Dawley rats were allocated (n=8/group) to sedentary control (HFC), aerobic exercise training (HFAX), or resistance exercise training (HFRX). Lean Zucker rats (LN, n=8) served as genetic controls while obese Zucker rats (n=24) were allocated (n=8/group) to sedentary control (FT), aerobic exercise training (FTAX), or resistance exercise training (FTRX). Following the 8-wk experimental period, animals underwent hindlimb perfusions and the insulin-stimulated red gastrocnemius was collected for viii analysis. High-fat diet induced impairments in insulin-stimulated rates of 3-MG transport in the Sprague Dawley rat were reversed by both aerobic and resistance training due to normalized IRS-1 pY and IRS-1 pS. IKK pS was similar across the HFRX, HFAX and NC animals. Insulin-stimulated rates of 3-MG transport and IRS-1 pY in the skeletal muscle of the FTRX, FTAX and LN groups were similar. Both aerobic and resistance training suppressed IKK pS in the skeletal muscle of the obese Zucker rat. These findings indicate that exercise training, regardless of mode, improves insulin signaling via suppressing IKK inflammation regardless of etiology of insulin resistance.
Download or read book Characterization of the Glucose Transport Mechanism Responsible for Mechanical Overload and Acute Injury stimulated Skeletal Muscle Glucose Uptake written by Parker Lance Evans and published by . This book was released on 2022 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: Skeletal muscle is a highly adaptable tissue. In response to stimuli such as resistance exercise training or trauma/injury, muscle glucose uptake is stimulated to fuel the energetic and biosynthetic demands of growth, repair, and regeneration processes. Understanding how muscle glucose uptake changes in response to resistance training or acute injury may advance new therapies for patients with type 2 diabetes or those with muscle trauma. Therefore, the overall objective of this dissertation was to determine the transport mechanism(s) used by skeletal muscle to increase glucose uptake in response to mechanical overload, a model of resistance exercise training, as well as in response to acute injury induced by barium chloride injection. AIM 1: Determine if glucose transporter 6 (GLUT6) is necessary for mechanical overload-stimulated skeletal muscle glucose uptake and hypertrophic growth. Mechanical overload stimulates an increase in GLUT6 levels in mouse skeletal muscle. However, its role in overload-stimulated muscle adaptations was unknown. Overload was induced by unilateral synergist muscle ablation surgery in mice lacking GLUT6 in all cells. After 5 days, muscle weight and glucose uptake were assessed. Neither overload-stimulated muscle growth nor glucose uptake were impaired in the mice lacking GLUT6. Lack of impairment in overload-induced glucose uptake and growth demonstrates that GLUT6 does not play an essential role in mediating overload-stimulated glucose uptake or growth in muscle. AIM 2: Determine if chemical damage-induced acute muscle injury stimulates glucose uptake via an adaptation intrinsic to skeletal muscle, and if so to determine the glucose transport mechanism(s) responsible for this effect. Glucose metabolism increases in skeletal muscle acute injured by chemical damage. Whether this is due to an adaptation intrinsic to the muscle tissue versus an in vivo factor(s) such as enhanced blood flow or nerve activity was unknown. Acute muscle injury was induced in mice by intramuscular injection of the chemical barium chloride. In isolated skeletal muscles, barium chloride stimulated glucose uptake was observed at 3-, 5-, 7- and 10-days post injection. This exciting ex-vivo glucose uptake finding demonstrated that chemical damage-induced acute injury stimulates muscle glucose uptake via an adaptation intrinsic to the muscle tissue. Additional key characteristics of the glucose transport mechanism underlying this adaptation included: 1) inhibitable by the facilitative glucose transporter inhibitor, cytochalasin B; 2) not dependent on glucose transporter 1 (GLUT1) expression in muscle cells; 3) not dependent on glucose transporter 1 (GLUT4) expression in muscle cells; and 4) not dependent on glucose transporter 6 (GLUT6) expression in any cell type. The findings presented in this dissertation are significant because they add to the growing body of evidence demonstrating that skeletal muscle tissue can metabolically adapt to stimuli such as chronic muscle overload or acute trauma/injury by stimulating a novel glucose transport mechanism intrinsic to the muscle tissue. Characterization of this transport mechanism(s) represents a key first step in the development of new therapies for individuals suffering from type 2 diabetes or acute muscle trauma/injury.
