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Table of Contents
Vol. 85, No. 2, 2007
Issue release date: May 2007
Section title: Appetite and Energy Balance
Neuroendocrinology 2007;85:71–80
(DOI:10.1159/000101694)

Corticosterone Impairs Insulin-Stimulated Translocation of GLUT4 in the Rat Hippocampus

Piroli G.G.a · Grillo C.A.a · Reznikov L.R.a · Adams S.a · McEwen B.S.b · Charron M.J.c · Reagan L.P.a
aDepartment of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine, Columbia, S.C., bHarold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, The Rockefeller University, New York, N.Y., and cDepartment of Biochemistry and Obstetrics and Gynecology and Women’s Health, Albert Einstein College of Medicine, Bronx, N.Y., USA

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Article / Publication Details

First-Page Preview
Abstract of Appetite and Energy Balance

Published online: April 05, 2007
Issue release date: May 2007

Number of Print Pages: 10
Number of Figures: 7
Number of Tables: 2

ISSN: 0028-3835 (Print)
eISSN: 1423-0194 (Online)

For additional information: http://www.karger.com/NEN

Abstract

Background: Exposure to stress levels of glucocorticoids produces physiological responses that are characteristic of type 2 diabetes, such as peripheral insulin resistance and impairment in insulin-stimulated trafficking of glucose transporter 4 (GLUT4) in muscle and fat. In the central nervous system, stress produces neuroanatomical and neurochemical changes in the hippocampus that are associated with cognitive impairments. Methods: In view of these observations, the current studies examined the effects of short-term (1 week) exposure of stress levels of glucocorticoids upon insulin receptor (IR) expression and signaling, including GLUT4 translocation, in the rat hippocampus. Results: One week of corticosterone (CORT) treatment produced insulin resistance in response to peripheral glucose challenge. In the hippocampus, IR expression was unchanged in CORT-treated rats as compared with vehicle-treated rats. However, insulin-stimulated phosphorylation of the IR, total Akt levels and total GLUT4 levels were reduced in CORT-treated rats when compared to controls. In addition, insulin-stimulated translocation of hippocampal GLUT4 to the plasma membrane was completely abolished in CORT-treated rats. Conclusions: These results demonstrate that in addition to eliciting peripheral insulin resistance, short-term CORT administration impairs insulin signaling in the rat hippocampus, effects that may contribute to the deleterious consequences of hypercortisolemic/hyperglycemic states observed in type 2 diabetes.

© 2007 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Appetite and Energy Balance

Published online: April 05, 2007
Issue release date: May 2007

Number of Print Pages: 10
Number of Figures: 7
Number of Tables: 2

ISSN: 0028-3835 (Print)
eISSN: 1423-0194 (Online)

For additional information: http://www.karger.com/NEN


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