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首页> 外文期刊>Cell metabolism >P53-induced adipose tissue inflammation is critically involved in the development of insulin resistance in heart failure
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P53-induced adipose tissue inflammation is critically involved in the development of insulin resistance in heart failure

机译：P53诱导的脂肪组织炎症与心力衰竭中胰岛素抵抗的发展密切相关

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Several clinical studies have shown that insulin resistance is prevalent among patients with heart failure, but the underlying mechanisms have not been fully elucidated. Here, we report a mechanism of insulin resistance associated with heart failure that involves upregulation of p53 in adipose tissue. We found that pressure overload markedly upregulated p53 expression in adipose tissue along with an increase of adipose tissue inflammation. Chronic pressure overload accelerated lipolysis in adipose tissue. In the presence of pressure overload, inhibition of lipolysis by sympathetic denervation significantly downregulated adipose p53 expression and inflammation, thereby improving insulin resistance. Likewise, disruption of p53 activation in adipose tissue attenuated inflammation and improved insulin resistance but also ameliorated cardiac dysfunction induced by chronic pressure overload. These results indicate that chronic pressure overload upregulates adipose tissue p53 by promoting lipolysis via the sympathetic nervous system, leading to an inflammatory response of adipose tissue and insulin resistance.
机译：几项临床研究表明，心力衰竭患者中普遍存在胰岛素抵抗，但其潜在机制尚未完全阐明。在这里，我们报告与心力衰竭相关的胰岛素抵抗的机制，其中涉及脂肪组织中p53的上调。我们发现压力超负荷显着上调了脂肪组织中p53的表达以及脂肪组织炎症的增加。慢性压力超负荷加速了脂肪组织中的脂肪分解。在压力超负荷的情况下，通过交感神经去脂抑制脂解作用显着下调了脂肪p53的表达和炎症，从而改善了胰岛素抵抗。同样，破坏脂肪组织中的p53激活可减轻炎症并改善胰岛素抵抗，但也可以缓解慢性压力超负荷引起的心脏功能障碍。这些结果表明，慢性压力超负荷通过交感神经系统促进脂解作用来上调脂肪组织p53，导致脂肪组织的炎症反应和胰岛素抵抗。

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