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首页> 外文期刊>Molecular medicine reports >Toll-like receptor 2 mediates deposition of collagen I in adipose tissue of high fat diet-induced obese mice
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Toll-like receptor 2 mediates deposition of collagen I in adipose tissue of high fat diet-induced obese mice

机译:Toll样受体2介导胶原蛋白I的沉积在高脂饮食诱导的肥胖小鼠的脂肪组织中

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摘要

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 TGF1 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)1, 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 TGF beta 1.
机译:肥胖症标志着胶原蛋白I在脂肪组织中标记。损害像受体(TLR)2涉及脂质代谢,但是TLR2和胶原蛋白之间的关联我仍然尚不清楚。本研究旨在探讨TLR2敲除对肥胖小鼠脂肪组织中胶原蛋白I的影响。 TLR2敲除和C57BL / 6J小鼠(4周龄)喂食正常的食物或高脂饮食16周。与来自瘦对照组织的脂肪组织相比,来自C57BL / 6J小鼠的小鼠高脂饮食增加了胶原I,TIMP1和TGF1水平和更低的MMP1水平。然而,除了增加的基质金属肽酶(MMP)1的水平增加,喂养高脂饮食的TLR2敲除小鼠的脂肪组织揭示了胶原I,TIMP金属肽酶抑制剂(TIMP)1的降低,以及转化生长因子(TGF)1。 。这些发现表明,在肥胖小鼠的脂肪组织中,TLR2参与胶原蛋白I的代谢,并且在MMP1,TIMP1和TGFβ1的代谢中可能表现出作用。

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