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内脏脂肪素在脂肪细胞前体细胞以及肥胖儿童和青少年中上调脂肪组织纤维化标志物。

The up-regulation of markers of adipose tissue fibrosis by visfatin in pre-adipocytes as well as obese children and adolescents.

机构信息

Department of Biochemistry, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran.

Metabolic Disorders Research Center, Endocrinology and Metabolism Molecular -Cellular Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran.

出版信息

Cytokine. 2020 Oct;134:155193. doi: 10.1016/j.cyto.2020.155193. Epub 2020 Jul 21.

Abstract

Adipocytes are surrounded by a three-dimensional network of extracellular matrix (ECM) proteins. Aberrant ECM accumulation and remodeling leads to adipose tissue fibrosis. Visfatin is one of the adipocytokines that is increased in obesity and is implicated in insulin resistance. The objective of this study was to investigate the effect of visfatin on major components of ECM remodeling. In this study, plasma levels of both endotrophin and visfatin in obese children and adolescents were significantly higher than those in control subjects and they showed a positive correlation with each other. Treatment of 3T3-L1 pre-adipocytes with visfatin caused significant up-regulation of Osteopontin (Opn), Collagen type VI (Col6), matrix metalloproteinases MMP-2 and MMP-9. By using inhibitors of major signaling pathways it was shown that visfatin exerted its effect on Col6a3 gene expression through PI3K, JNK, and NF-кB pathways, while induced Opn gene expression via PI3K, JNK, MAPK/ERK, and NOTCH1. Our conclusion is that, the relationship between visfatin, endotrophin and insulin resistance parameters in obesity as well as increased expression of ECM proteins by visfatin suggests adipose tissue fibrosis as a mechanism for devastating effects of visfatin in obesity.

摘要

脂肪细胞被细胞外基质 (ECM) 蛋白的三维网络所包围。异常的 ECM 积累和重塑导致脂肪组织纤维化。内脏脂肪素是肥胖症中增加的脂肪细胞因子之一,与胰岛素抵抗有关。本研究的目的是研究内脏脂肪素对 ECM 重塑主要成分的影响。在这项研究中,肥胖儿童和青少年的血浆内脂素和内脏脂肪素水平明显高于对照组,且相互呈正相关。用内脏脂肪素处理 3T3-L1 前脂肪细胞会导致骨桥蛋白 (Opn)、VI 型胶原 (Col6)、基质金属蛋白酶 MMP-2 和 MMP-9 的显著上调。通过使用主要信号通路的抑制剂,表明内脏脂肪素通过 PI3K、JNK 和 NF-кB 通路对 Col6a3 基因表达发挥作用,而通过 PI3K、JNK、MAPK/ERK 和 NOTCH1 通路诱导 Opn 基因表达。我们的结论是,肥胖症中内脏脂肪素、内脂素与胰岛素抵抗参数之间的关系以及内脏脂肪素对 ECM 蛋白表达的增加表明脂肪组织纤维化是内脏脂肪素在肥胖症中产生破坏性影响的机制。

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