Role of Omentin, Vaspin, Cardiotrophin-1, TWEAK and NOV/CCN3 in Obesity and Diabetes Development.
作者： Xavier Escoté , Saioa Gómez-Zorita , Miguel López-Yoldi , Iñaki Milton-Laskibar , Alfredo Fernández-Quintela
DOI: 10.3390/IJMS18081770
关键词: Cytokine TWEAK 、 Type 2 diabetes 、 Insulin 、 White adipose tissue 、 Endocrinology 、 Diabetes mellitus 、 Adipose tissue 、 Insulin resistance 、 Biology 、 Adipokine 、 Internal medicine
摘要: Adipose tissue releases bioactive mediators called adipokines. This review focuses on the effects of omentin, vaspin, cardiotrophin-1, Tumor necrosis factor-like Weak Inducer Apoptosis (TWEAK) and nephroblastoma overexpressed (NOV/CCN3) obesity diabetes. Omentin is produced by stromal-vascular fraction visceral adipose tissue. Obesity reduces omentin serum concentrations secretion in adults adolescents. adipokine regulates insulin sensitivity, but its clinical relevance has to be confirmed. Vaspin subcutaneous tissues. levels are higher obese subjects, as well subjects showing resistance or type 2 Cardiotrophin-1 an with a similar structure cytokines from interleukin-6 family. There some controversy regarding regulation cardiotrophin-1 -subjects, gene expression down-regulated white diet-induced mice. It also shows anti-obesity hypoglycemic properties. TWEAK potential regulator low-grade chronic inflammation characteristic obesity. seem not directly related adiposity, metabolic factors play critical role regulation. Finally, strong correlation been found between plasma NOV/CCN3 concentration fat mass. improves actions.
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