Horm Metab Res 1999; 31(10): 546-552
DOI: 10.1055/s-2007-978793
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© Georg Thieme Verlag Stuttgart · New York

Differential Effects of Palmitate on Glucose Uptake in Rat-1 Fibroblasts and 3T3-L1 Adipocytes

I. Usui, T. Haruta, Y. Takata, M. Iwata, T. Uno, A. Takano, E. Ueno, O. Ishibashi, H. Ishihara, T. Wada, T. Sasaoka, M. Kobayashi
  • From the First Department of Medicine, Toyama Medical and Pharmaceutical University, Sugitani, Toyama, Japan
Further Information

Publication History

1999

1999

Publication Date:
20 April 2007 (online)

Abstract

Non-esterified fatty acids are thought to be one of the causes for insulin resistance. However, the molecular mechanism of fatty acid-induced insulin resistance is not clearly known. In this study, we first examined the effect of palmitate on insulin signaling in 3T3-L1 adipocytes. We found that 1h treatment with 1 mmol/l palmitate had no effect on insulin binding, tyrosine phosphorylation of insulin receptors, 185 kDa proteins and Shc, and PI3 kinase activity in 3T3-L1 adipocytes. Then, the effects of palmitate on MAP kinase activity and glucose uptake in fully differentiated 3T3-L1 adipocytes were compared with those in poorly differentiated 3T3-L1 cells and in HIRc-B cells. Palmitate treatment had no effect on MAP kinase activity in fully differentiated 3T3-L1 adipocytes, while it inhibited MAP kinase in poorly differentiated 3T3-L1 cells and HIRc-B cells. Glucose transport in 3T3-L1 adipocytes treated with palmitate for 1 h, 4 h and 16 h was higher than that in control cells, but palmitate treatment caused a rightward shift of the insulin-dose responsive curve for glucose uptake in HIRc-B cells. Palmitate treatment did not significantly affect basal and insulin-stimulated GLUT4 translocation. When the cells were treated with PD98059, a specific MEK inhibitor, insulin-stimulated glucose uptake was not affected in 3T3-L1 adipocytes, while it was almost completely inhibited in HIRc-B cells. These results suggest the primary effect of palmitate on adipocytes may not involve insulin resistance of adipocytes themselves.

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