Fetuin-A: a novel link between obesity and related complications.
Fetuin-A: a novel link between obesity and related complications.
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DOI：
10.1038/ijo.2014.203
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发表时间：
2015-01-01
影响因子：
4.9
通讯作者：
Varady, K. A.
中科院分区：
文献类型：
--
作者：
Trepanowski, J. F.;Mey, J.;Varady, K. A.
胎球蛋白-A（FetA）是一种64-kDa的糖蛋白，由肝脏和脂肪组织分泌。循环FetA在肥胖和相关疾病中升高，包括2型糖尿病、非酒精性脂肪肝疾病和代谢综合征; FetA相关参数，钙蛋白颗粒，与超重/肥胖慢性肾病患者的血管钙化高度相关。FetA水平也与胰岛素敏感性和葡萄糖耐量受损有关。越来越多的证据表明，升高的FetA水平导致血糖控制受损，因为FetA涉及胰岛素受体信号传导、toll样受体4活化、巨噬细胞迁移和极化、脂肪细胞功能障碍、肝细胞三酰甘油积累以及肝脏炎症和纤维化的损害。减肥、有氧运动、二甲双胍和吡格列酮均被证明可有效降低FetA水平。
Fetuin-A (FetA) is a 64-kDa glycoprotein that is secreted from both the liver and adipose tissue. Circulating FetA is elevated in obesity and related disorders including type 2 diabetes mellitus, nonalcoholic fatty liver disease and the metabolic syndrome; and a FetA-related parameter, caliciprotein particle, is highly relevant to vascular calcification in overweight/obese patients with chronic kidney disease. FetA level is also associated with impaired insulin sensitivity and glucose tolerance. Accumulating evidence suggests that elevated FetA level causes impaired glycemic control, as FetA has been implicated in impairment of insulin receptor signaling, toll-like receptor 4 activation, macrophage migration and polarization, adipocyte dysfunction, hepatocyte triacylglycerol accumulation and liver inflammation and fibrosis. Weight loss, aerobic exercise, metformin and pioglitazone have each been shown to be effective for reducing FetA level.