Effects of Exercise Training on Skeletal Muscle Insulin Signaling and Inflammation in Two Rodent Models of Insulin Resistance PDF Download
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Author: Lindsea Burns
Publisher:
ISBN:
Category :
Languages : en
Pages : 48
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Book Description
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.
Author: Lindsea Burns
Publisher:
ISBN:
Category :
Languages : en
Pages : 48
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Book Description
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.
Author: Neal Washburn
Publisher:
ISBN:
Category :
Languages : en
Pages : 186
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Book Description
Author: Junghoon Kim
Publisher:
ISBN:
Category :
Languages : en
Pages : 202
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Book Description
Author: Hans-Georg Joost
Publisher: Humana Press
ISBN: 9781627030670
Category : Science
Languages : en
Pages : 0
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Book Description
In recent years, human studies have made enormous contributions towards an understanding of the genetic basis of diabetes mellitus; however, most of the experimentation needed for the invention and testing of novel therapeutic approaches cannot be performed in humans. Thus, there is no alternative to appropriate animal models. In Animal Models in Diabetes Research, expert researchers explore the current status of the most important models and procedures in order to provide a timely resource in experimental diabetology. The first half of the volume serves as a comprehensive overview on our current knowledge of the pathogenesis and pathophysiology of diabetes in animal models through a series of reviews in model strains. The book then continues with vital, established protocols that are employed in the characterization and study of animal models of diabetes. As a volume in the highly successful Methods in Molecular BiologyTM series, this work contains the type of detailed description and key implementation advice necessary to achieve successful results. Authoritative and cutting-edge, Animal Models in Diabetes Research delivers essential content that will be an important resource to advance diabetes research in the years to come.
Author: Alan R. Saltiel
Publisher: Springer Science & Business Media
ISBN: 0387722041
Category : Medical
Languages : en
Pages : 223
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Book Description
More than 18 million people in the United States have diabetes mellitus, and about 90% of these have the type 2 form of the disease. This book attempts to dissect the complexity of the molecular mechanisms of insulin action with a special emphasis on those features of the system that are subject to alteration in type 2 diabetes and other insulin resistant states. It explores insulin action at the most basic levels, through complex systems.
Author: Clinton R. Bruce
Publisher:
ISBN:
Category : Exercise
Languages : en
Pages : 462
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Book Description
Author: George Grunberger
Publisher: CRC Press
ISBN: 0203302958
Category : Science
Languages : en
Pages : 485
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Book Description
With contributions from the leading researchers in the field, this volume brings together the latest studies on insulin action and signal transduction to provide a state-of-the-art reference for graduate researchers and students in diabetes and endocrinology. Insulin Signaling is a comprehensive study of the regulation of molecular events by insulin at a cellular level, utilizing experimental techniques ranging from molecular systems through phenotypic expression in transgenic and knockout models.
Author: Emily Dunford
Publisher:
ISBN:
Category :
Languages : en
Pages : 0
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Book Description
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.
Author: Birgitte Falbe Vind
Publisher:
ISBN:
Category :
Languages : en
Pages : 172
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Book Description
Author: Mark Hargreaves
Publisher: Human Kinetics
ISBN: 9780736041034
Category : Energy metabolism
Languages : en
Pages : 320
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Book Description
A comprehensive reference for biochemists, sport nutritionists, exercise physiologists, and graduate students in those disciplines. Provides information on the metabolic processes that take place during exercise, examining in depth the mobilization and utilization of substrates during physical activity. Focuses primarily on the skeletal muscle, but also discusses the roles of the liver and adipose tissue. Annotation copyright by Book News, Inc., Portland, OR
