Regulation of SOCS-3, OB, GLUT4 and PPARgamma gene expression by insulin and dexamethasone in porcine primary adipocyte.
- Author:
Haowei ZHANG
1
;
Jiangwei WU
;
Bo WANG
;
Zhen LÜ
;
Gongshe YANG
Author Information
1. College of Animal Science and Technology, Northwest A & F University, Yangling 712100, China.
- Publication Type:Journal Article
- MeSH:
Adipocytes;
cytology;
metabolism;
Animals;
Cells, Cultured;
Dexamethasone;
pharmacology;
Glucose Transporter Type 4;
biosynthesis;
genetics;
Insulin;
pharmacology;
Insulin Resistance;
Leptin;
biosynthesis;
genetics;
PPAR gamma;
biosynthesis;
genetics;
Suppressor of Cytokine Signaling 3 Protein;
Suppressor of Cytokine Signaling Proteins;
biosynthesis;
genetics;
Swine
- From:
Chinese Journal of Biotechnology
2008;24(8):1354-1360
- CountryChina
- Language:Chinese
-
Abstract:
Swine is an ideal model for diabetes studies. Insulin and insulin resistance are closely related with diabetes. To investigate the effect of SOCS-3 in insulin resistance, porcine primary adipocyte was treated with insulin (100 nmol/L) and dexamethasone (300 nmol/L) to induce insulin resistance. The simi-quantitative PCR results suggested that insulin increased GLUT4, PPARgamma and SOCS-3 gene expression in primary culture porcine adipocytes and no change of OB gene expression. Under insulin resistance conditions, SOCS-3 and OB gene expression were up-regulated, whereas GLUT4 and PPARgamma gene expression were down-regulated in primary porcine adipocytes. The overexpression of PPARgamma gene resulted in the increase of GLUT4 expression by insulin. Different expression levels of SOCS-3 determined the inhibitory effects of insulin signaling. Induction of insulin resistance by dexamethasone was not only due to inhibition of glucose transportation, but also repression of insulin signaling. SOCS-3 might be a potential gene to block the insulin resistance.
