Accumulating evidence suggests that mitochondrial dysfunction and adipocyte differentiation promote lipid accumulation in the development of obesity and diabetes. Curcumin is an active ingredient extracted from Curcuma longa that has been shown to exhibit antioxidant and anti-inflammatory potency in metabolic disorders. However, the underlying mechanisms of curcumin in adipocytes remain largely unexplored. We studied the effects of curcumin on adipogenic differentiation and mitochondrial oxygen consumption and analysed the possible mechanisms. 3T3-L1 preadipocytes were used to assess the effect of curcumin on differentiation of adipocytes. The Mito Stress Test measured by Seahorse XF Analyzer was applied to investigate the effect of curcumin on mitochondrial oxygen consumption in 3T3-L1 adipocytes. The effect of curcumin on the morphology of both white and brown adipose tissue (WAT and BAT) was evaluated in a high-fat diet-induced obese mice model. We found that curcumin dose-dependently (10, 20 and 35 µM) induced adipogenic differentiation and the intracellular fat droplet accumulation. Additionally, 10 µM curcumin remarkably enhanced mature adipocyte mitochondrial respiratory function, specifically, accelerating basic mitochondrial respiration, ATP production and uncoupling capacity via the regulation of peroxisome proliferator-activated receptor γ (PPARγ) (p < 0.01). Curcumin administration also attenuated the morphological changes in adipose tissues in high-fat diet-induced obese mice. Moreover, curcumin markedly increased the mRNA and protein expressions of mitochondrial uncoupling protein 1 (UCP1), PPARγ, peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) and PR domain protein 16 (PRDM16) in vivo and in vitro. Collectively, the results demonstrate that curcumin promotes the adipogenic differentiation of preadipocytes and mitochondrial oxygen consumption in 3T3-L1 mature adipocytes by regulating UCP1, PRDM16, PPARγ and PGC-1α expression.

越来越多的证据表明，线粒体功能障碍和脂肪细胞分化促进肥胖症和糖尿病发展过程中的脂质蓄积。姜黄素是从姜黄中提取的有效成分已显示在代谢紊乱中具有抗氧化和抗发炎的功效。然而，姜黄素在脂肪细胞中的潜在机制仍在很大程度上未被探索。我们研究了姜黄素对脂肪形成分化和线粒体耗氧量的影响，并分析了可能的机制。使用3T3-L1前脂肪细胞评估姜黄素对脂肪细胞分化的影响。使用Seahorse XF分析仪测量的线粒体压力测试用于研究姜黄素对3T3-L1脂肪细胞线粒体耗氧量的影响。在高脂饮食诱导的肥胖小鼠模型中评估了姜黄素对白色和棕色脂肪组织（WAT和BAT）形态的影响。我们发现姜黄素剂量依赖性（10，20和35 µM）诱导成脂分化和细胞内脂肪滴积聚。此外，10 µM姜黄素可显着增强成熟的脂肪细胞线粒体呼吸功能，特别是通过调节过氧化物酶体增殖物激活受体γ（PPARγ）来加速基本线粒体呼吸，ATP产生和解偶联能力（p <0.01）。姜黄素的施用还减轻了高脂饮食诱导的肥胖小鼠脂肪组织的形态变化。此外，姜黄素在体内和体外显着增加线粒体解偶联蛋白1（UCP1），PPARγ，过氧化物酶体增殖物激活的受体-γcoactivator-1α（PGC-1α）和PR域蛋白16（PRDM16）的mRNA和蛋白表达。总体而言，结果表明姜黄素通过调节UCP1，PRDM16，PPARγ和PGC-1α的表达，促进3T3-L1成熟脂肪细胞中前脂肪细胞的脂肪形成分化和线粒体耗氧量。