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首页> 外文期刊>Cell metabolism >Celastrol Protects against Obesity and Metabolic Dysfunction through Activation of a HSF1-PGC1 alpha Transcriptional Axis
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Celastrol Protects against Obesity and Metabolic Dysfunction through Activation of a HSF1-PGC1 alpha Transcriptional Axis

机译：Celastrol通过激活HSF1-PGC1 alpha转录轴来预防肥胖和代谢功能异常

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Altering the balance between energy intake and expenditure is a potential strategy for treating obesity and metabolic syndrome. Nonetheless, despite years of progress in identifying diverse molecular targets, biological-based therapies are limited. Here we demonstrate that heat shock factor 1 (HSF1) regulates energy expenditure through activation of a PGC1 alpha-dependent metabolic program in adipose tissues and muscle. Genetic modulation of HSF1 levels altered white fat remodeling and thermogenesis, and pharmacological activation of HSF1 via celastrol was associated with enhanced energy expenditure, increased mitochondrial function in fat and muscle and protection against obesity, insulin resistance, and hepatic steatosis during high-fat diet regimens. The beneficial metabolic changes elicited by celastrol were abrogated in HSF1 knockout mice. Overall, our findings identify the temperature sensor HSF1 as a regulator of energy metabolism and demonstrate that augmenting HSF1 via celastrol represents a possible therapeutic strategy to treat obesity and its myriad metabolic consequences.
机译：改变能量摄入和支出之间的平衡是治疗肥胖症和代谢综合征的潜在策略。尽管如此，尽管在识别各种分子靶标方面取得了多年进展，但基于生物的疗法仍然受到限制。在这里，我们证明了热休克因子1（HSF1）通过激活脂肪组织和肌肉中PGC1α依赖性代谢程序来调节能量消耗。 HSF1水平的遗传调节改变了白色脂肪的重塑和生热作用，而通过Celastrol激活HSF1的药理作用与增加能量消耗，增加脂肪和肌肉中的线粒体功能以及在肥胖，高脂饮食方案中预防肥胖，胰岛素抵抗和肝脂肪变性有关。 。在HSF1基因敲除小鼠中，取消了由Celastrol引起的有益的代谢变化。总体而言，我们的发现将温度传感器HSF1识别为能量代谢的调节剂，并证明通过Celastrol增加HSF1代表了治疗肥胖症及其多种代谢后果的可能治疗策略。

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