Lone Jameel, Choi Jae Heon, Kim Sang Woo, Yun Jong Won
Department of Biotechnology, Daegu University, Kyungsan, Kyungbuk 712-714, Republic of Korea.
Department of Biotechnology, Daegu University, Kyungsan, Kyungbuk 712-714, Republic of Korea.
J Nutr Biochem. 2016 Jan;27:193-202. doi: 10.1016/j.jnutbio.2015.09.006. Epub 2015 Sep 21.
Recent advances have been made in the understanding of pharmacological and dietary agents that contribute to browning of white adipose tissue in order to combat obesity by promoting energy expenditure. Here, we show that curcumin induces browning of 3T3-L1 and primary white adipocytes via enhanced expression of brown fat-specific genes. Curcumin-induced browning in white adipocytes was investigated by determining expression levels of brown adipocyte-specific genes/proteins by real-time reverse transcriptase polymerase chain reaction, immunoblot analysis and immunocytochemical staining. Curcumin increased mitochondrial biogenesis, as evidenced by transmission electronic microscopic detection and enhanced expression of proteins involved in fat oxidation. Cucurmin also increased protein levels of hormone-sensitive lipase and p-acyl-CoA carboxylase, suggesting its possible role in augmentation of lipolysis and suppression of lipogenesis. Increased expression of UCP1 and other brown adipocyte-specific markers was possibly mediated by curcumin-induced activation of AMP-activated protein kinase (AMPK) based on the fact that inhibition of AMPK by dorsomorphin abolished expression of PRDM16, UCP1 and peroxisome proliferator-activated receptor gamma co-activator 1-alpha while the activator 5-Aminoimidazole-4-carboxamide ribonucleotide elevated expression of these brown marker proteins. Our findings suggest that curcumin plays a dual modulatory role in inhibition of adipogenesis as well as induction of the brown fat-like phenotype and thus may have potential therapeutic implications for treatment of obesity.
在理解有助于白色脂肪组织褐变的药理和饮食因素方面,为了通过促进能量消耗来对抗肥胖,最近取得了一些进展。在此,我们表明姜黄素通过增强棕色脂肪特异性基因的表达来诱导3T3-L1和原代白色脂肪细胞的褐变。通过实时逆转录聚合酶链反应、免疫印迹分析和免疫细胞化学染色来测定棕色脂肪细胞特异性基因/蛋白质的表达水平,从而研究姜黄素诱导白色脂肪细胞褐变的情况。姜黄素增加了线粒体生物合成,这通过透射电子显微镜检测以及参与脂肪氧化的蛋白质表达增强得到证明。姜黄素还增加了激素敏感性脂肪酶和对 - 酰基辅酶A羧化酶的蛋白质水平,表明其在增强脂肪分解和抑制脂肪生成中可能发挥的作用。基于以下事实,即通过 dorsomorphin 抑制 AMP 活化蛋白激酶(AMPK)消除了PRDM16、UCP1和过氧化物酶体增殖物激活受体γ共激活因子1 - α的表达,而激活剂5 - 氨基咪唑 - 4 - 甲酰胺核糖核苷酸提高了这些棕色标记蛋白的表达,UCP1和其他棕色脂肪细胞特异性标记物表达的增加可能是由姜黄素诱导的AMPK活化介导的。我们的研究结果表明,姜黄素在抑制脂肪生成以及诱导棕色脂肪样表型方面发挥双重调节作用,因此可能对肥胖症的治疗具有潜在的治疗意义。