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

First Author  Erol E Year  2004
Journal  Am J Physiol Endocrinol Metab Volume  287
Issue  5 Pages  E977-82
PubMed ID  15198933 Mgi Jnum  J:95402
Mgi Id  MGI:3525951 Doi  10.1152/ajpendo.00139.2004
Citation  Erol E, et al. (2004) Nonacute effects of H-FABP deficiency on skeletal muscle glucose uptake in vitro. Am J Physiol Endocrinol Metab 287(5):E977-82
abstractText  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.
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