期刊
BIOCHEMICAL PHARMACOLOGY
卷 68, 期 10, 页码 1929-1937出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.bcp.2004.07.036
关键词
adipocytes; glucose uptake; insulin; phosphatidylinositol 3-kinase; Akt; GLUT4
Caffeine inhibits insulin-induced glucose uptake in rat adipocytes and also decreases insulin sensitivity, including whole-body glucose disposal and glucose uptake in skeletal muscle, during a euglycemic-hyperinsulinemic clamp in human. However, the mechanism by which caffeine decreases the insulin sensitivity is not still clear. We found that pre-treatment with caffeine inhibited the insulin-induced 2-deoxy-D-[1-H-3]glucose uptake in a concentration-dependent manner in mouse preadipose MC-3T3-G2/PA6 cells differentiated into mature adipose cells. Caffeine also suppressed insulin-induced GLUT4 translocation in the differentiated cells. Although caffeine did not alter insulin-induced activation of PI3K and protein kinase C-zeta (PKC), an isoform of atypical PKC, which is reported to have an important role in insulin-induced GLUT4 translocation, we found that insulin-induced phosphorylation and activation of Akt were blocked by pre-treatment with caffeine. Inhibition of insulin-induced 2-deoxy-D-[1-H-3]glucose uptake by caffeine was also observed in primary cultured brown adipocytes in a concentration-dependent manner. These results may, in part, explain the ability of caffeine to decrease insulin sensitivity. (C) 2004 Elsevier Inc. All rights reserved.
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