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Toll 样受体 2 介导高脂饮食诱导肥胖小鼠脂肪组织中 I 型胶原的沉积。

Toll‑like receptor 2 mediates deposition of collagen I in adipose tissue of high fat diet‑induced obese mice.

机构信息

Endocrinology Department, First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121000, P.R. China.

出版信息

Mol Med Rep. 2018 Apr;17(4):5958-5963. doi: 10.3892/mmr.2018.8590. Epub 2018 Feb 12.

DOI:10.3892/mmr.2018.8590
PMID:29436650
Abstract

Obesity is marked by deposition of collagen I in adipose tissue. Toll like receptor (TLR)2 is involved in lipid metabolism, however the association between TLR2 and collagen I remains unclear. The present study was designed to investigate the effect of TLR2 knockout on collagen I in adipose tissue in obese mice. TLR2 knockout and C57BL/6J mice (aged 4 weeks) were fed normal chow or a high‑fat‑diet for 16 weeks. Compared with adipose tissue from lean controls, that from C57BL/6J mice fed a high‑fat diet had increased levels of collagen I, TIMP1 and TGFβ1 and lower levels of MMP1. However, adipose tissue from TLR2 knockout mice fed a high‑fat diet revealed decreased levels of collagen I, TIMP metallopeptidase inhibitor (TIMP)1, and transforming growth factor (TGF)β1, in addition to increased levels of matrix metallopeptidase (MMP)1. These findings suggest that, in the adipose tissue of obese mice, TLR2 is involved in the metabolism of collagen I and may exhibit a role in the metabolism of MMP1, TIMP1 and TGFβ1.

摘要

肥胖的特征是脂肪组织中 I 型胶原的沉积。Toll 样受体 2(TLR2)参与脂质代谢,然而 TLR2 与 I 型胶原之间的关系尚不清楚。本研究旨在探讨 TLR2 敲除对肥胖小鼠脂肪组织中 I 型胶原的影响。TLR2 敲除和 C57BL/6J 小鼠(4 周龄)分别给予正常饲料或高脂肪饲料喂养 16 周。与瘦对照组相比,高脂肪饮食喂养的 C57BL/6J 小鼠的脂肪组织中 I 型胶原、TIMP1 和 TGFβ1 水平升高,MMP1 水平降低。然而,高脂肪饮食喂养的 TLR2 敲除小鼠的脂肪组织中 I 型胶原、TIMP 金属蛋白酶抑制剂(TIMP)1 和转化生长因子(TGF)β1 水平降低,同时 MMP1 水平升高。这些发现表明,在肥胖小鼠的脂肪组织中,TLR2 参与 I 型胶原的代谢,并且可能在 MMP1、TIMP1 和 TGFβ1 的代谢中发挥作用。

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