Zhang Haowei, Wu Jiangwei, Wang Bo, Lü Zhen, Yang Gongshe
College of Animal Science and Technology, Northwest A & F University, Yangling 712100, China.
Sheng Wu Gong Cheng Xue Bao. 2008 Aug;24(8):1354-60.
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.
猪是糖尿病研究的理想模型。胰岛素和胰岛素抵抗与糖尿病密切相关。为了研究SOCS-3在胰岛素抵抗中的作用,用胰岛素(100 nmol/L)和地塞米松(300 nmol/L)处理猪原代脂肪细胞以诱导胰岛素抵抗。半定量PCR结果表明,胰岛素增加了原代培养猪脂肪细胞中GLUT4、PPARγ和SOCS-3基因的表达,而OB基因表达无变化。在胰岛素抵抗条件下,原代猪脂肪细胞中SOCS-3和OB基因表达上调,而GLUT4和PPARγ基因表达下调。PPARγ基因的过表达导致胰岛素诱导的GLUT4表达增加。SOCS-3的不同表达水平决定了胰岛素信号传导的抑制作用。地塞米松诱导的胰岛素抵抗不仅是由于葡萄糖转运的抑制,还包括胰岛素信号传导的抑制。SOCS-3可能是一个潜在的阻断胰岛素抵抗的基因。