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Non-alcoholic fatty liver disease (NAFLD) results from triglyceride accumulation within the liver and some of them advances to non-alcoholic steatohepatitis (NASH). It is important to note that in NAFLD development, hepatic  de novo  lipogenesis (DNL) derives from excess carbohydrates and fats under a condition of excess energy through β-oxidation. As a main regulator for DNL, sterol regulatory element-binding protein 1 ( Srebp-1 ) forms complex with progesterone receptor membrane component 1 ( Pgrmc1 ). To investigate whether  Pgrmc1  may have a notable effect on DNL  via  SREBP-1 activation, we generated  Pgrmc1  knockout (KO) mice and fed a high fat diet for one month. High-fat-fed  Pgrmc1  KO mice showed a substantial increase in levels of hepatic TG accumulation, and they were predisposed to NAFLD when compared to WT mice. Loss of  Pgrmc1  increased mature SREBP-1 protein level, suggesting that induction of hepatic steatosis in  Pgrmc1  KO mice might be triggered by  de novo  lipogenesis. Moreover,  Pgrmc1  KO mice were also more vulnerable to early stage of NASH, showing high levels of alanine aminotransferase, obesity-linked pro-inflammatory cytokines, and fibrosis markers. This is interesting because  Pgrmc1  involves with the first step in regulating the hepatic de novo lipogenesis under an excess energy condition.

Loss of progesterone receptor membrane component 1 promotes hepatic steatosis via the induced de novo lipogenesis