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Glucose transporters: cellular links to hyperglycemia in insulin resistance and diabetes.

Abstract
Abnormal expression and/or function of mammalian hexose transporters contribute to the hallmark hyperglycemia of diabetes. Due to different roles in glucose handling, various organ systems possess specific transporters that may be affected during the diabetic state. Diabetes has been associated with higher rates of intestinal glucose transport, paralleled by increased expression of both active and facilitative transporters and a shift in the location of transporters within the enterocyte, events that occur independent of intestinal hyperplasia and hyperglycemia. Peripheral tissues also exhibit deregulated glucose transport in the diabetic state, most notably defective translocation of transporters to the plasma membrane and reduced capacity to clear glucose from the bloodstream. Expression of renal active and facilitative glucose transporters increases as a result of diabetes, leading to elevated rates of glucose reabsorption. However, this may be a natural response designed to combat elevated blood glucose concentrations and not necessarily a direct effect of insulin deficiency. Functional foods and nutraceuticals, by modulation of glucose transporter activity, represent a potential dietary tool to aid in the management of hyperglycemia and diabetes.
AuthorsDanielle M Stringer, Peter Zahradka, Carla G Taylor
JournalNutrition reviews (Nutr Rev) Vol. 73 Issue 3 Pg. 140-54 (Mar 2015) ISSN: 1753-4887 [Electronic] United States
PMID26024537 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
Copyright© The Author(s) 2015. Published by Oxford University Press on behalf of the International Life Sciences Institute. All rights reserved. For Permissions, please e-mail: [email protected].
Chemical References
  • Glucose Transport Proteins, Facilitative
  • Insulin
  • Glucose
Topics
  • Animals
  • Diabetes Mellitus (metabolism)
  • Glucose (metabolism)
  • Glucose Transport Proteins, Facilitative
  • Humans
  • Hyperglycemia (metabolism)
  • Insulin (metabolism)
  • Insulin Resistance (physiology)
  • Mice

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