Diet-induced thermogenesis (DIT) is crucial for maintaining body weight homeostasis, and the role of dietary fatty acids in modulating DIT is essential. However, the underlying mechanism of fatty acid regulated diet-induced thermogenesis remains elusive. Utilizing the diet- and genetic ablation-induced obese mice models, we found that the C16 unsaturated fatty acids, trans-palmitoleic acid (TPA) and cis-palmitoleic acid (CPA), significantly increased the energy expenditure by promoting the thermogenesis of brown adipose tissues and the production of beige cells in white adipose. As a result, there is a significant reduction in the occurrence of obesity, associated hepatic steatosis and hyperglycemia. Notably, TPA exhibited more potent effects on promoting DIT and alleviating obesity than CPA did. Using inhibitor and gene deletion mice models, we unveiled that TPA acted as a signaling molecule to play a biological function, which could be sensed by the hypothalamic FFAR1 to activate the sympathetic nervous system in promoting adipose tissue thermogenesis. Together, these results demonstrate the underlying mechanism of free fatty acids associated-DIT and will provide fresh insights into the roles of trans-fatty acids in the development of obesity.

中文翻译：

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反式棕榈油酸通过下丘脑 FFAR1 信号传导促进脂肪产热以减少肥胖

饮食诱导产热 (DIT) 对于维持体重稳态至关重要，而膳食脂肪酸在调节 DIT 中的作用至关重要。然而，脂肪酸调节饮食诱导产热的潜在机制仍然难以捉摸。利用饮食和基因消融诱导的肥胖小鼠模型，我们发现C16不饱和脂肪酸、反式棕榈油酸（TPA）和顺式棕榈油酸（CPA）通过促进棕色脂肪的产热显着增加能量消耗组织和白色脂肪中米色细胞的产生。结果，肥胖、相关肝脂肪变性和高血糖的发生率显着减少。值得注意的是，TPA 在促进 DIT 和减轻肥胖方面表现出比 CPA 更有效的作用。利用抑制剂和基因缺失小鼠模型，我们揭示了TPA作为信号分子发挥生物学功能，可以被下丘脑FFAR1感知，激活交感神经系统，促进脂肪组织产热。总之，这些结果证明了游离脂肪酸相关 DIT 的潜在机制，并将为反式脂肪酸在肥胖发展中的作用提供新的见解。