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网膜素、内脏脂肪素、心肌营养素-1、肿瘤坏死因子样弱凋亡诱导因子及肾母细胞瘤过度表达基因/富半胱氨酸蛋白3在肥胖和糖尿病发生发展中的作用

Role of Omentin, Vaspin, Cardiotrophin-1, TWEAK and NOV/CCN3 in Obesity and Diabetes Development.

作者信息

Escoté Xavier, Gómez-Zorita Saioa, López-Yoldi Miguel, Milton-Laskibar Iñaki, Fernández-Quintela Alfredo, Martínez J Alfredo, Moreno-Aliaga María J, Portillo María P

机构信息

Department of Nutrition, Food Sciences and Physiology, University of Navarra, 31008 Pamplona, Spain.

Centre for Nutrition Research, University of Navarra, 31008 Pamplona, Spain.

出版信息

Int J Mol Sci. 2017 Aug 15;18(8):1770. doi: 10.3390/ijms18081770.

DOI:10.3390/ijms18081770
PMID:28809783
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5578159/
Abstract

Adipose tissue releases bioactive mediators called adipokines. This review focuses on the effects of omentin, vaspin, cardiotrophin-1, Tumor necrosis factor-like Weak Inducer of Apoptosis (TWEAK) and nephroblastoma overexpressed (NOV/CCN3) on obesity and diabetes. Omentin is produced by the stromal-vascular fraction of visceral adipose tissue. Obesity reduces omentin serum concentrations and adipose tissue secretion in adults and adolescents. This adipokine regulates insulin sensitivity, but its clinical relevance has to be confirmed. Vaspin is produced by visceral and subcutaneous adipose tissues. Vaspin levels are higher in obese subjects, as well as in subjects showing insulin resistance or type 2 diabetes. Cardiotrophin-1 is an adipokine with a similar structure as cytokines from interleukin-6 family. There is some controversy regarding the regulation of cardiotrophin-1 levels in obese -subjects, but gene expression levels of cardiotrophin-1 are down-regulated in white adipose tissue from diet-induced obese mice. It also shows anti-obesity and hypoglycemic properties. TWEAK is a potential regulator of the low-grade chronic inflammation characteristic of obesity. TWEAK levels seem not to be directly related to adiposity, and metabolic factors play a critical role in its regulation. Finally, a strong correlation has been found between plasma NOV/CCN3 concentration and fat mass. This adipokine improves insulin actions.

摘要

脂肪组织会释放被称为脂肪因子的生物活性介质。本综述聚焦于网膜素、内脏脂肪素、心肌营养素-1、肿瘤坏死因子样凋亡微弱诱导剂(TWEAK)和成神经细胞瘤过度表达蛋白(NOV/CCN3)对肥胖和糖尿病的影响。网膜素由内脏脂肪组织的基质血管部分产生。肥胖会降低成年人和青少年的网膜素血清浓度以及脂肪组织分泌量。这种脂肪因子可调节胰岛素敏感性,但其临床相关性尚待证实。内脏脂肪素由内脏和皮下脂肪组织产生。肥胖受试者以及存在胰岛素抵抗或2型糖尿病的受试者体内的内脏脂肪素水平较高。心肌营养素-1是一种脂肪因子,其结构与白细胞介素-6家族的细胞因子相似。关于肥胖受试者中心肌营养素-1水平的调节存在一些争议,但在饮食诱导的肥胖小鼠的白色脂肪组织中,心肌营养素-1的基因表达水平下调。它还具有抗肥胖和降血糖特性。TWEAK是肥胖所特有的低度慢性炎症的潜在调节因子。TWEAK水平似乎与肥胖程度无直接关联,代谢因素在其调节中起关键作用。最后,已发现血浆NOV/CCN3浓度与脂肪量之间存在强相关性。这种脂肪因子可改善胰岛素作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75ed/5578159/58e2b054682d/ijms-18-01770-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75ed/5578159/ea9d3e28f783/ijms-18-01770-g002.jpg
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