The Effect Of Uqcrc1 On Adipogenesis And The Induction Of Beige-like Adipocytes

To date,great growing upsurge interest is putting into the adipocytes which are associated with obesity and metabolism disease.Adipocytes,best known for fat storage,can also suppress weight gain and fight against metabolic disease through the specialized heat-producing action.Adipose tissue plays profound effects on physiology and pathophysiology due to its energy storage and expenditure.Adipocytes are broadly divided into brown and white fat cells.Brown adipocytes produce heat uncoupling the respiration,counteracting obesity,whereas the white fat cells store chemical energy.Excessive energy intake without an equal expenditure promotes adipocyte hyperplasia and adiposity.Brown or beige adipocytes utilize a high mitochondrial content and high mitochondrial Ucp1 to uncouple respiration and dissipate chemical energy as heat.Thus,the classical brown or thermogenesis adipose draws a lot attention to figure out the mechanism,and also the brown-like(beige or brite)within white adipose.Ubiquinol-cytochrome c reductase core protein 1(Uqcrcl,nuclear DNA encoded),which encodes a subunit of mitochondrial respiratory complex ?,is a momentous components of the respiratory chain.Overexpression of Uqcrcl led to a upregulated in related proteins,causing elevated respiration rates and energy storage with decreased ATP production in the white adipose tissue(WAT)on one hand,energy dissipation with increased ATP production in the brown adipose tissue(BAT)on the other hand.In this regard,we hypothesis that the regulation of Uqcrcl gene might influence respiration status.Rare work of this gene in vivo or in vitro was published.Thus,great growing upsurge interest is putting into the thermogenesis adipocytes,coinciding with a more important role in vitro cell lineage,3T3-L1,due to the potential differentiating into adipocytes.To induce thermogenesis adipocytes,an additional treatment of IBMX,ROSI and ISO was used following a standard differentiation program.The lentivirus-mediated system was used to silence Uqcrc1 gene expression in 3T3-L1 pre-adipocytes.Expression of Uqcrc1,as estimated by real-time quantitative PCR(RT-qPCR),was reduced by 90%compared to control and LV-Scr-sh transduced cells.Substantially decreased expression of fatty acid binding protein 4(Fabp4),Oil-Red-O staining was implemented.This reprogram treatment enhanced the Ucp1 mRNA expression,the thermogenic key transcription factors,including C/EBP?,Prdm16 and Pgc-1?,and beige-like enriched markers(Cd137,Cited1,Tmem26,Tbx1).Silencing Uqcrc1 via a lentivirus-mediated system suppresses the induction of thermogenesis adipocytes and the beigeing program.Ucpl,thermogenic key transcription factors,beige-like enriched markers were down-regulated expression in mRNA level to different extent after silencing Uqcrc1 in 3T3-L1 and underwent induction of thermogenesis phenotype treatment.These data provide a foundation for rodent,even mammalian,with therapeutic potential.