HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ranalletta, M. Articles by Charron, M. J. Search for Related Content PubMed PubMed Citation Articles by Ranalletta, M. Articles by Charron, M. J. Social Bookmarking                What's this?

Altered Hepatic and Muscle Substrate Utilization Provoked by GLUT4 Ablation

¹ Department of Biochemistry, Albert Einstein College of Medicine, Bronx, New York
² Department of Medicine, Columbia University New York, New York, New York

Studies were conducted to explore altered substrate utilization and metabolism in GLUT4 null mice. Liver fatty acid synthase mRNA and fatty acid synthesis rates were dramatically increased in GLUT4 null mice compared with control mice and were supported by increased rates of the pentose phosphate pathway oxidative phase and sterol regulatory binding protein mRNA expression. Increased GLUT2 protein content, glucokinase mRNA, and glucose-6-phosphate in GLUT4 null mice may provide substrate for the enhanced fatty acid synthesis. Increased fatty acid synthesis, however, did not lead to hepatic triglyceride accumulation in GLUT4 null mice because of increased hepatic triglyceride secretion rates. GLUT4 null mice rapidly cleared orally administered olive oil, had reduced serum triglyceride concentrations in the fed and the fasted state, and increased skeletal muscle lipoprotein lipase when compared with controls. Oleate oxidation rates were increased in GLUT4 null skeletal muscle in association with mitochondrial hyperplasia/hypertrophy. This study demonstrated that GLUT4 null mice had increased hepatic glucose uptake and conversion into triglyceride for subsequent use by muscle. The ability of GLUT4 null mice to alter hepatic carbohydrate and lipid metabolism to provide proper nutrients for peripheral tissues may explain (in part) their ability to resist diabetes when fed a normal diet.

CiteULike    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				F. Backhed, J. K. Manchester, C. F. Semenkovich, and J. I. Gordon From the Cover: Mechanisms underlying the resistance to diet-induced obesity in germ-free mice PNAS, January 16, 2007; 104(3): 979 - 984. [Abstract] [Full Text] [PDF]

				C.-H. Lee, P. Olson, A. Hevener, I. Mehl, L.-W. Chong, J. M. Olefsky, F. J. Gonzalez, J. Ham, H. Kang, J. M. Peters, et al. PPAR{delta} regulates glucose metabolism and insulin sensitivity PNAS, February 28, 2006; 103(9): 3444 - 3449. [Abstract] [Full Text] [PDF]