FITM2 deficiency results in ER lipid accumulation, ER stress, reduced apolipoprotein B lipidation, and VLDL triglyceride secretion in vitro and in mouse liver.
Haizhen WangCyrus NikainJaime AmengualMaxwell La ForestYong YuMeng C WangRussell WattsRichard LehnerYunping QiuMin CaiIrwin J KurlandIra J GoldbergSujith RajanM Mahmood HussainJeffrey L BrodskyEdward A FisherPublished in: bioRxiv : the preprint server for biology (2023)
The results suggest that FITM2 contributes to VLDL lipidation, especially when newly synthesized hepatic TG is in abundance. In addition to its fundamental importance in VLDL assembly, the results also suggest that under dysmetabolic conditions, FITM2 may be a limiting factor that ultimately contributes to non-alcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH).