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Defective Phosphatidylglycerol Remodeling Causes Hepatopathy, Linking Mitochondrial Dysfunction to Hepatosteatosis.
BACKGROUND & AIMS: Obesity promotes the development of nonalcoholic fatty liver diseases (NAFLD), yet not all obese patients develop NAFLD. The underlying causes for this discrepancy remain elusive. LPGAT1 is an acyltransferase that catalyzes the remodeling of phosphatidylglycerol (PG), a mitochondrial phospholipid implicated in various metabolic diseases. Here we investigated the role of LPGAT1 in regulating the onset of diet-induced obesity (DIO) and its related hepatosteatosis, since polymorphisms of the LPGAT1 gene promoter was strongly associated with susceptibility to obesity in Pima Indians.
METHODS: Mice with whole-body knockout of LPGAT1 were generated to investigate the role of PG remodeling in NAFLD.
RESULTS: LPGAT1 deficiency protected mice from DIO, but led to hepatopathy, insulin resistance, and NAFLD as a consequence of oxidative stress, mtDNA depletion, and mitochondrial dysfunction.
CONCLUSIONS: This study identified an unexpected role of PG remodeling in obesity, linking mitochondrial dysfunction to NAFLD.
METHODS: Mice with whole-body knockout of LPGAT1 were generated to investigate the role of PG remodeling in NAFLD.
RESULTS: LPGAT1 deficiency protected mice from DIO, but led to hepatopathy, insulin resistance, and NAFLD as a consequence of oxidative stress, mtDNA depletion, and mitochondrial dysfunction.
CONCLUSIONS: This study identified an unexpected role of PG remodeling in obesity, linking mitochondrial dysfunction to NAFLD.
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