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This Article Full Text Full Text (PDF) All Versions of this Article: 287/5/E977    most recent 00139.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Erol, E. Articles by Binas, B. Search for Related Content PubMed PubMed Citation Articles by Erol, E. Articles by Binas, B.

Nonacute effects of H-FABP deficiency on skeletal muscle glucose uptake in vitro

¹Department of Pathobiology, College of Veterinary Medicine, Texas A&M University, College Station 77843; ³Division of Cardiology, University of Texas Houston Medical School, Houston, Texas 77030; and ²Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06536

Submitted 23 March 2004 ; accepted in final form 10 June 2004

Heart-type fatty acid-binding protein (H-FABP) is required for high rates of skeletal muscle long-chain fatty acid (LCFA) oxidation and esterification. Here we assessed whether H-FABP affects soleus muscle glucose uptake when measured in vitro in the absence of LCFA. Wild-type and H-FABP null mice were fed a standard chow or high-fat diet before muscle isolation. With the chow, the mutation increased insulin-dependent deoxyglucose uptake by 141% (P < 0.01) at 0.02 mU/ml of insulin but did not cause a significant effect at 2 mU/ml of insulin; skeletal muscle triglyceride and long-chain acyl-CoA (LCA-CoA) levels remained normal. With the high-fat diet, the mutation increased insulin-dependent deoxyglucose uptake by 190% (P < 0.01) at 2 mU/ml of insulin, thus partially preventing insulin resistance, and it completely prevented the threefold (P < 0.001) diet-induced increase of muscle triglyceride levels; however, muscle LCA-CoA levels showed little or no reduction. With both diets, the mutation reduced the basal (insulin-independent) soleus muscle deoxyglucose uptake by 28% (P < 0.05). These results establish a close relation between FABP-dependent lipid pools and insulin sensitivity and indicate the existence of a nonacute, antagonistic, and H-FABP-dependent fatty acid regulation of basal and insulin-dependent muscle glucose uptake.

heart-type fatty acid-binding protein; insulin; insulin resistance

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