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3 edition of Glycemic regulation of the rat skeletal muscle glucose transport system found in the catalog.

Glycemic regulation of the rat skeletal muscle glucose transport system

Dimitrios Peter Dimitrakoudis

Glycemic regulation of the rat skeletal muscle glucose transport system

by Dimitrios Peter Dimitrakoudis

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  • 17 Currently reading

Published by National Library of Canada = Bibliothèque nationale du Canada in Ottawa .
Written in English


Edition Notes

SeriesCanadian theses = Thèses canadiennes
The Physical Object
FormatMicroform
Pagination2 microfiches : negative.
ID Numbers
Open LibraryOL14754455M
ISBN 100315785012

Christina Werner, Michael Schwarzer, in The Scientist's Guide to Cardiac Metabolism, Glucose uptake and glycogen. Glucose transport in myocytes is driven by the translocation of monosaccharide transporters (GLUT-4 and GLUT-1) to the sarcolemma. Insulin-mediated GLUT-4 is the major glucose transporter in cardiac and skeletal muscle [7].In contrast, GLUT-1 shows a much lower glucose. Activation of glucose transport in skeletal muscle by phospholipase C and phorbol ester. Evaluation of the regulatory roles of protein kinase C and calcium.

  The prevalence of type 2 diabetes (T2D) is rapidly increasing, and effective strategies to manage and prevent this disease are urgently needed. Resistance training (RT) promotes health benefits through increased skeletal muscle mass and qualitative adaptations, such as enhanced glucose transport and mitochondrial oxidative capacity. In particular, mitochondrial adaptations triggered by Cited by:   We investigated the acute effect of hyperglycemia on 3- O -methylglucose transport in isolated rat epitrochlearis muscles. High levels of glucose (20 mmol/1) induced an ∼ twofold increase in the rate of glucose transport when compared with muscles exposed to a low level of glucose (8 mmol/1) (P Cited by:

glucose uptake, glycogen synthesis, and the activity ratio of glycogen synthase, i.e., synthase activity (mi-nus glucosephosphate)/synthase activity (plus glu-cosephosphate at saturating concentrations). The results suggest that prior exercise enhances both the sensitivity of the glucose transport system to insulin and glycogen synthesis. Hydrogen (H 2) acts as a therapeutic r, there are few reports on H 2 function in other capacities in diabetes mellitus (DM). Therefore, in this study, we investigated the role of H 2 in glucose transport by studying cultured mouse C2C12 cells and human hepatoma Hep-G2 cells in vitro, in addition to three types of diabetic mice [Streptozotocin (STZ)-induced type 1 diabetic Cited by:


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Glycemic regulation of the rat skeletal muscle glucose transport system by Dimitrios Peter Dimitrakoudis Download PDF EPUB FB2

Abstract. A primary human skeletal muscle culture (HSMC) system, which retains cellular integrity and insulin responsiveness for glucose transport was employed to evaluate glucose transport regulation.

As previously reported, cells cultured from non-insulin-dependent diabetic (NIDDM) subjects displayed significant reductions in both basal and acute insulin-stimulated transport compared to nondiabetic Cited by: The entry of glucose into muscle cells is achieved primarily via a carrier-mediated system consisting of protein transport molecules.

GLUT-1 transporter isoform is normally found in the sarcolemmal (SL) membrane and is thought to be involved in glucose transport under basal by:   Walker PS, Ramlal T, Donovan JA, Doering TP, Sandra A, Klip A, Pessin JE () Insulin and glucose-dependent regulation of the glucose transport system in the rat L6 skeletal muscle cell line.

J Biol Chem – Google ScholarCited by: Future endeavors focused on determining the molecular and cellular factors that are responsible for the ability of exercise training to elicit beneficial effects on systemic glucose homeostasis, skeletal muscle glucose transport and/or skeletal muscle glucose metabolism should seek to fill in these critical knowledge by: 1.

Aerobic exercise training and resistance exercise training are both well-known for their ability to improve human health; especially in individuals with type 2 diabetes.

However, there are critical differences between these two main forms of exercise training and the adaptations that they induce in the body that may account for their beneficial by: 1.

Glucose transport in skeletal muscle follows saturation kinetics, and most reports have shown that exercise and insulin increase glucose transport through an increase in the maximal velocity of transport (V max) without an appreciable change in the substrate concentration at which glucose transport is half-maximal, orK m (43, 52, 86,87).Cited by: tal understanding of the glucose transport system in skeletal muscle.

To test the hypothesis that the translocation of glucose transporters is a major mechanism by which physical exercise increases glucose uptake, initial ex-periments studied skeletal muscles obtained from rats that were exercised by running on a motorized rodent treadmill.

regulation of glucose transport activity and expression in white- and red-enriched skeletal muscle from control, dia- betic, and insulin-treated diabetic rats. The data presented in this study demonstrate a skeletal muscle fiber type-specific regulation of GLUT4 expression as well as a dissociation.

Theincrease inskeletal muscle glucose transport with acuteexercise issimilartotheincrease seenwithmaximum insulin stimulation (37,39).Theincreases, however, appear toinvolvedifferent pathways. Although insulin isthought to actviatheinsulin receptor tyrosine kinase, asdiscussed earlier, Treadway etal.(42)found noincrease inreceptor.

Regulation of Skeletal Muscle Glucose Uptake During Exercise. There are three sites of regulation of skeletal muscle glucose uptake in vivo: glucose delivery to the skeletal muscle cells, surface membrane permeability to glucose (i.e., glucose transport), and Cited by: In rat skeletal muscle, acute treatment with insulin in vivo increases glucose-transport activity and the number of specific cytochalasin B-binding sites at the plasma membrane.

In mildly diabetic (streptozocin-induced) rats, the number of cytochalasin B-binding sites is decreased in total membranes, and preferentially in the plasma by:   Skeletal muscle is the primary tissue responsible for insulin-dependent glucose uptake in vivo; therefore, glucose uptake by this tissue plays an important role in determining glycemia.

Glucose uptake in muscle occurs by a system of facilitated diffusion involving at least two distinct glucose transporters, GLUT-1 and GLUTCited by: glucose transport regulation.

Emphasis is placed on the use of the mitochondrial uncoupler dinitrophenol to investigate mediators of this alternative signalling pathway in muscle cells, a line used to characterize physiological responses in muscle such as glucose transport.

The glucose transporter in the plasma membrane of rat skeletal muscle has been identified by two approaches. In one, the transporter was detected as the polypeptide that was differentially labeled by photolysis with [3 H]cytochalasin B in the presence of l - and d-glucose.[3 H]Cytochalasin B is a high-affinity ligand for the transporter that is displaced by by:   Exercise and insulin regulation of glucose transport.

A proposed model for the signaling pathways mediating exercise- and insulin-induced skeletal muscle glucose transport is Cited by: In mammals, skeletal muscle is the primary target for the stimulation of glucose transport by a variety of activators.

These include the hormone insulin and stimuli which increase energy demand. In skeletal muscle, GLUT4 translocation to the plasmamembrane and glucose transport are known to be stimulated by AMPK Expression of Author: Mirko Magnone, Laura Emionite, Lucrezia Guida, Tiziana Vigliarolo, Laura Sturla, Sonia Spinelli, Amb.

Skeletal muscle plays important role in the regulation of whole-body metabolism. In skeletal muscle, uptakes of glucose and fatty acid from circulation are Cited by: After running training, which increased GLUT-4 protein content in rat skeletal muscle by glucose transport.

Exercise improves glucose control by increasing insulin sensitivity and non–insulin-dependent glucose uptake in skeletal muscle. There is also evidence that energy turnover (i.e., the oxidation of glucose and fatty acids) during muscle contraction is important for preventing the accumulation of metabolic intermediates that contribute to insulin resistance (7).Cited by: 3.

This may reflect the differential regulation of insulin- and AMPK-induced glucose transport in skeletal muscle cells, with reports showing that AS phosphorylation is Cited by: 7.In book: The Endocrine System in Sports and Exercise, pp - and decreased glucose transport in skeletal muscle.

Total content of muscle GLUT4 protein is not affected by. Hypoglycemia is the leading limiting factor in glycemic management of insulin-treated diabetes. Skeletal muscle is the predominant site of insulin-mediated glucose disposal.

Our study used a crossover design to test to what extent insulin-induced hypoglycemia affects glucose uptake in skeletal muscle and whether hypoglycemia counterregulation modulates insulin and catecholamine Cited by: 4.