Mammalian target of rapamycin complex 1 and FoxO1 in the transcriptional control of lipolysis and de novo lipogenesis

Purpose of reviewPostprandial suppression of lipolysis in adipose tissue and stimulation of de novo lipogenesis (DNL) in the liver by insulin are essential for the metabolic homeostasis in the mammalian organism. The mechanism of coregulation of lipolysis and DNL is not clear.Recent findingsInsulin controls both lipolysis and DNL at the level of transcription via the same mammalian target of rapamycin complex 1 (mTORC1) and FoxO1-mediated signaling pathways.SummarymTORC1 suppresses lipolysis in adipose tissue and activates DNL in the liver, whereas FoxO1 has the opposite effect. Individual inputs of either mTORC1 or FoxO1 in the regulation of lipid metabolism may be difficult to evaluate because of the cross talk between these pathways.