Diabetes 51:1737-1744, 2002
© 2002 by the American Diabetes Association, Inc.
Humoral Regulation of Resistin Expression in 3T3-L1 and Mouse Adipose Cells
Nobuhiro Shojima1,
Hideyuki Sakoda2,
Takehide Ogihara1,
Midori Fujishiro1,
Hideki Katagiri3,
Motonobu Anai2,
Yukiko Onishi2,
Hiraku Ono2,
Kouichi Inukai4,
Miho Abe1,
Yasushi Fukushima1,
Masatoshi Kikuchi2,
Yoshitomo Oka3, and
Tomoichiro Asano1
1 Department of Internal Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
2 Institute for Adult Disease, Asahi Life Foundation, Tokyo, Japan
3 Department of Internal Medicine, University of Tohoku, Sendai, Japan
4 Fourth Department of Internal Medicine, Saitama Medical School, Saitama, Japan
Resistin is a hormone secreted by adipocytes that acts on skeletal muscle myocytes, hepatocytes, and adipocytes themselves, reducing their sensitivity to insulin. In the present study, we investigated how the expression of resistin is affected by glucose and by mediators known to affect insulin sensitivity, including insulin, dexamethasone, tumor necrosis factor- (TNF- ), epinephrine, and somatropin. We found that resistin expression in 3T3-L1 adipocytes was significantly upregulated by high glucose concentrations and was suppressed by insulin. Dexamethasone increased expression of both resistin mRNA and protein 2.5- to 3.5-fold in 3T3-L1 adipocytes and by 70% in white adipose tissue from mice. In contrast, treatment with troglitazone, a thiazolidinedione antihyperglycemic agent, or TNF- suppressed resistin expression by 80%. Epinephrine and somatropin were both moderately inhibitory, reducing expression of both the transcript and the protein by 3050% in 3T3-L1 adipocytes. Taken together, these data make it clear that resistin expression is regulated by a variety of hormones and that cytokines are related to glucose metabolism. Furthermore, they suggest that these factors affect insulin sensitivity and fat tissue mass in part by altering the expression and eventual secretion of resistin from adipose cells.

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Copyright © 2002 by the American Diabetes Association.
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