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首页> 外文期刊>Cytokine >TNF-α reduces g0s2 expression and stimulates lipolysis through PPAR-γ inhibition in 3T3-L1 adipocytes
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TNF-α reduces g0s2 expression and stimulates lipolysis through PPAR-γ inhibition in 3T3-L1 adipocytes

机译：TNF-α通过抑制3T3-L1脂肪细胞中的PPAR-γ降低g0s2表达并刺激脂解

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摘要

Tumor necrosis factor-α (TNF-α) is a multifunctional cytokine that acts as a mediator of obesity-linked insulin resistance (IR). It is commonly accepted that macrophage-derived TNF-α acts in a paracrine manner on adjacent adipocytes, induces lipolysis, which contributes to obesity-linked hyperglycemia. Several studies suggested that G0/. G1 switch gene 2 (g0s2) was up-regulated during adipogenesis, and its protein could be degraded in response to TNF-α stimulation. The aim of the present work was to investigate the transcriptional regulation of g0s2 by TNF-α stimulation. In this study, 3T3-L1 pre-adipocytes were differentiated, and treated with TNF-α for 24. h. The effects of TNF-α on lipolysis and lipase expression were then examined. Our results revealed that TNF-α exerted dose- and time-dependent lipolytic effects, which could be partially reversed by overexpression of g0s2 and peroxisome proliferator-activated receptor-γ (ppar-γ). In addition, TNF-α treatment significantly reduced the expression of adiponectin, ppar-γ, hormone-sensitive Lipase (hsl), adipose triglyceride lipase (atgl) as well as ATGL co-factors. Interestingly, TNF-α significantly decreased adiponectin and PPAR-γ protein levels, while treatment with the proteasomal inhibitor MG-132 maintained PPAR-γ levels. Degradation of PPAR-γ almost completely abolished the binding of PPAR-γ to the g0s2 promoter in adipocytes treated with TNF-α. We propose that proteasomal degradation of PPAR-γ and the reduction of g0s2 content are permissive for prolonged TNF-α induced lipolysis.
机译：肿瘤坏死因子-α（TNF-α）是一种多功能细胞因子，可作为肥胖相关胰岛素抵抗（IR）的介质。通常认为巨噬细胞源性TNF-α以旁分泌的方式作用于相邻的脂肪细胞，诱导脂肪分解，从而导致肥胖相关的高血糖症。多项研究表明，G0 /。 G1开关基因2（g0s2）在脂肪形成过程中被上调，其蛋白可响应TNF-α刺激而降解。本工作的目的是研究TNF-α刺激下g0s2的转录调控。在这项研究中，分化了3T3-L1前脂肪细胞，并用TNF-α处理了24小时。然后检查了TNF-α对脂解和脂肪酶表达的影响。我们的研究结果表明，TNF-α发挥剂量和时间依赖性的脂解作用，而g0s2和过氧化物酶体增殖物激活的受体-γ（ppar-γ）的过表达可部分逆转它。此外，TNF-α处理可显着降低脂联素，ppar-γ，激素敏感性脂肪酶（hsl），甘油三酸酯脂肪酶（atgl）以及ATGL辅助因子的表达。有趣的是，TNF-α显着降低了脂联素和PPAR-γ的蛋白水平，而蛋白酶体抑制剂MG-132的治疗则维持了PPAR-γ的水平。在用TNF-α处理的脂肪细胞中，PPAR-γ的降解几乎完全消除了PPAR-γ与g0s2启动子的结合。我们建议延长TNF-α诱导的脂解允许PPAR-γ的蛋白酶体降解和g0s2含量的减少。

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