Pharmacological stimulation of adipose tissue remodeling and thermogenesis to increase energy expenditure is expected to be a viable therapeutic strategy for obesity. Berberine has been reported to have pharmacological activity in adipose tissue to anti-obesity, while the mechanism remains unclear. Here, we observed that berberine significantly reduced the body weight and insulin resistance of high-fat diet mice by promoting the distribution of brown adipose tissue and thermogenesis. We have further demonstrated that berberine activated energy metabolic sensing pathway AMPK/SIRT1 axis to increase the level of PPARγ deacetylation, which leads to promoting adipose tissue remodeling and increasing the expression of the thermogenic protein UCP-1. These findings suggest that berberine that enhances the AMPK/SIRT1 pathway can act as a selective PPARγ activator to promote adipose tissue remodeling and thermogenesis. This study proposes a new mechanism for the regulation of berberine in adipose tissue and offers a great prospect for berberine in obesity treatment

中文翻译：

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小檗碱通过 AMPK/SIRT1 通路调节 PPARγ 的去乙酰化以促进脂肪组织重塑和产热

脂肪组织重塑和产热以增加能量消耗的药理学刺激有望成为肥胖症的可行治疗策略。据报道，小檗碱在脂肪组织中具有抗肥胖的药理活性，但机制仍不清楚。在这里，我们观察到黄连素通过促进棕色脂肪组织的分布和产热显着降低高脂饮食小鼠的体重和胰岛素抵抗。我们进一步证明了小檗碱激活能量代谢传感通路AMPK/SIRT1轴以增加PPARγ去乙酰化水平，从而促进脂肪组织重塑并增加产热蛋白UCP-1的表达。这些发现表明，增强 AMPK/SIRT1 通路的小檗碱可以作为选择性 PPARγ 激活剂来促进脂肪组织重塑和产热。本研究提出了调节脂肪组织中黄连素的新机制，为黄连素在肥胖治疗中的应用提供了广阔前景