摘要
脂肪量及肥胖相关基因(FTO)被认定为肥胖关联最强最确切的基因,其单核苷酸多态性变异是导致肥胖的主要原因,通常来讲,其通过与其他肥胖相关基因、细胞因子发生相互作用,从而影响体内脂质的代谢,达到调控体脂量的目的。但是,FTO的很多作用机制尚未得到确切证实。本文综述了FTO通过调控IRX3、IRX5的表达,致使白色脂肪细胞内UCP1增多,变成米色脂肪细胞,从而影响能量代谢反应的相关生理机制。FNDC5是新近发现的肌肉相关因子,受到细胞因子PGC-1的诱导激活后,可表达Irisin蛋白,从而促使棕色脂肪细胞的UCP-1表达增加,同时促进细胞转化,提高解偶联呼吸作用的产热耗能反应。PRDM16被冠以"棕色脂肪细胞开关"一名,可激活棕色脂肪细胞关键特征,增强线粒体作用、解耦连呼吸作用及调控PGC-1a和UCP1等的表达;抑制富集白脂肪的几种基因的m RNA水平如resistin和serpin3ak的表达,达到强有力地干预棕色脂肪细胞的分化、代谢及转化反应的效果。
FTO gene was identified as the strongest and most accurate gene in obesity. FTO single nucleotide polymorphism variation is the main reason of the obesity, its affect lipid metabolism through interact with other obesity related genes and cytokines, and then control the amount of body fat. Many mechanisms of FTO have not been elucidated. This study summarize that through regulates the expression of IRX3 and IRX5, FTO can result in UCP1 transcription up-regulation in WAT then change into beige adipocytes, thus affecting the energy metabolism. FNDC5 is a newly discovered muscle-related factor, which can be induced by cytokine PGC-1 to expression irisin protein, then promote UCP-1 expression in brown adipocytes, and enhance the cell transformation and uncoupling respiration to strengthen thermogenesis. PRDM16 is called ＂switch＂ of brown fat cells, it can activate the key characteristics of brown adipose cells, enhance mitochondrial function, uncoupling respiration and regulating the expression of PGC-1α and UCP1; then inhibit the m RNA levels of several genes, such as resistin and serpin3ak, that enrich WAT, which exhibits a strong intervention in BAT differentiation, metabolism and transformation.
出处
《生命的化学》
CAS
CSCD
2017年第6期971-979,共9页
Chemistry of Life
基金
湖南省教育厅科学研究项目(16K064)
长沙市科技局资助项目(kq1602015)
湖南省芦笋研究开发中心芦笋产业联合研究开发基金
