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Adipose KLF15 Controls Lipid Handling to Adapt to Nutrient Availability

机译:脂肪KLF15控制脂质处理以适应营养供应

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Summary Adipose tissue stores energy in the form of triglycerides. The ability to regulate triglyceride synthesis and breakdown based on nutrient status (e.g., fed versus fasted) is critical for physiological homeostasis and dysregulation of this process can contribute to metabolic disease. Whereas much is known about hormonal control of this cycle, transcriptional regulation is not well understood. Here, we show that the transcription factor Kruppel-like factor 15 (KLF15) is critical for the control of adipocyte lipid turnover. Mice lacking Klf15 in adipose tissue (AK15KO) display decreased adiposity and are protected from diet-induced obesity. Mechanistic studies suggest that adipose KLF15 regulates key genes of triglyceride synthesis and inhibits lipolytic action, thereby promoting lipid storage in an insulin-dependent manner. Finally, AK15KO mice demonstrate accelerated lipolysis and altered systemic energetics (e.g., locomotion, ketogenesis) during fasting conditions. Our study identifies adipose KLF15 as an essential regulator of adipocyte lipid metabolism and systemic energy balance.
机译:小结脂肪组织以甘油三酸酯的形式存储能量。基于营养状况(例如,进食还是禁食)调节甘油三酸酯合成和分解的能力对于生理稳态是至关重要的,并且该过程的失调可导致代谢疾病。尽管人们对该周期的激素控制了解很多,但对转录调控的了解却很少。在这里,我们显示出转录因子Kruppel样因子15(KLF15)对于控制脂肪细胞脂质更新至关重要。脂肪组织中缺乏Klf15的小鼠(AK15KO)的脂肪减少,并且可以避免饮食引起的肥胖。机理研究表明,脂肪KLF15调节甘油三酸酯合成的关键基因并抑制脂解作用,从而以胰岛素依赖的方式促进脂质的储存。最后,AK15KO小鼠在禁食期间表现出加速的脂解作用和改变的全身能量(例如,运动,生酮作用)。我们的研究确定脂肪KLF15是脂肪细胞脂质代谢和全身能量平衡的重要调节剂。

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