SOCS-1 deficiency does not prevent diet-induced insulin resistance
SOCS-1 deficiency does not prevent diet-induced insulin resistance
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DOI：
10.1016/j.bbrc.2008.09.158
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发表时间：
2008-12-12
影响因子：
3.1
通讯作者：
Kahn, C. Ronald
中科院分区：
文献类型：
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作者：
Emanuelli, Brice;Macotela, Yazmin;Kahn, C. Ronald
肥胖与炎症和细胞因子信号抑制因子（SOCS）蛋白表达增加有关，SOCS蛋白抑制细胞因子和胰岛素信号传导。因此，减少SOCS的表达可以预防肥胖引起的胰岛素抵抗的发生。利用SOCS-1敲除小鼠，我们研究了SOCS-1在高脂肪饮食（HFD）诱导的胰岛素抵抗发展中的作用。HFD组的SOCS-1基因敲除小鼠体重增加70%，附睾脂肪垫质量增加2.3倍，肝脏脂质含量增加。与此同时，白色脂肪组织中瘦素和巨噬细胞标志物CD68 mRNA表达升高，肝脏中SREBP1c和FAS mRNA表达升高。在葡萄糖和胰岛素耐量试验受损的SOCS-1缺陷小鼠中，HFD也诱导高血糖。因此，尽管SOCS蛋白在肥胖相关的胰岛素抵抗中发挥作用，但单独缺乏SOCS-1并不能够预防富含脂肪的饮食诱导的胰岛素抵抗。(C) 2008爱思唯尔公司版权所有。
Obesity is associated with inflammation and increased expression of suppressor of cytokine signaling (SOCS) proteins, which inhibit cytokine and insulin signaling. Thus, reducing SOCS expression could prevent the development of obesity-induced insulin resistance. Using SOCS-1 knockout mice, we investigated the contribution of SOCS-1 in the development of insulin resistance induced by a high-fat diet (HFD). SOCS-1 knockout mice on HFD gained 70% more weight, displayed a 2.3-fold increase in epididymal fat pads mass and increased hepatic lipid content. This was accompanied by increased mRNA expression of leptin and the macrophage marker CD68 in white adipose tissue and of SREBP1c and FAS in liver. HFD also induced hyperglycemia in SOCS-1 deficient mice with impairment of glucose and insulin tolerance tests. Thus, despite the role of SOCS proteins in obesity-related insulin resistance, SOCS-1 deficiency alone is not able to prevent insulin resistance induced by a diet rich in fat. (C) 2008 Elsevier Inc. All rights reserved.