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首页> 外文期刊>Journal of Cellular Physiology >Mild mitochondrial uncoupling induces HSL/ATGL‐independent lipolysis relying on a form of autophagy in 3T3‐L1 adipocytes
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Mild mitochondrial uncoupling induces HSL/ATGL‐independent lipolysis relying on a form of autophagy in 3T3‐L1 adipocytes

机译：轻微的线粒体解偶联诱发奥软/ ATGL还是独立的脂解作用依赖于一种形式自噬在3 t3 L1脂肪细胞

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摘要

Obesity is characterized by an excessive triacylglycerol accumulation in white adipocytes. Various mechanisms allowing the tight regulation of triacylglycerol storage and mobilization by lipid droplet‐associated proteins as well as lipolytic enzymes have been identified. Increasing energy expenditure by inducing a mild uncoupling of mitochondria in adipocytes might represent a putative interesting anti‐obesity strategy as it reduces the adipose tissue triacylglycerol content (limiting alterations caused by cell hypertrophy) by stimulating lipolysis through yet unknown mechanisms, limiting the adverse effects of adipocyte hypertrophy. Herein, the molecular mechanisms involved in lipolysis induced by a mild uncoupling of mitochondria in white 3T3‐L1 adipocytes were characterized. Mitochondrial uncoupling‐induced lipolysis was found to be independent from canonical pathways that involve lipolytic enzymes such as HSL and ATGL. Finally, enhanced lipolysis in response to mitochondrial uncoupling relies on a form of autophagy as lipid droplets are captured by endolysosomal vesicles. This new mechanism of triacylglycerol breakdown in adipocytes exposed to mild uncoupling provides new insights on the biology of adipocytes dealing with mitochondria forced to dissipate energy.
机译：肥胖的特点是过度三酰甘油在白色脂肪细胞堆积。各种机制允许严格监管三酰甘油的存储和动员脂滴蛋白以及相关量分解脂肪的酶已确定。增加能量消耗通过诱导温和脂肪细胞中线粒体解偶联的可能代表一个假定的有趣的反肥胖策略,因为它减少了脂肪组织三酰甘油的内容(限制改变由细胞肥大)通过刺激引起的脂类分解通过未知的机制,限制脂肪细胞的不利影响肥大。参与脂类分解引起的轻微线粒体解偶联的白色3 t3 L1脂肪细胞的特征。解偶联诱导脂解作用被发现独立于规范涉及的途径分解脂肪的酶如奥软和ATGL。增强线粒体脂类分解反应解偶联依赖一种自噬作为脂质水滴被endolysosomal囊泡。这种新的机制的三酰甘油崩溃在脂肪细胞暴露于轻度解偶联提供脂肪细胞的生物学处理新见解与线粒体被迫能量消散。

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