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Fatty Liver Disease and Multi-System Complications | EK28


The role of TMEM55B in NAFLD onset and progression


Mar 22, 2021 12:00am ‐ Mar 22, 2021 12:00am

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The role of TMEM55B in NAFLD onset and progression Yuanyuan Qin1, Flora Ting1, Aras Mattis2, Ronald M. Krauss1, Marisa W. Medina1 1. Department of Pediatrics, University of California San Francisco, Oakland, CA 94609 2. Department of Pathology, University of California San Francisco, San Francisco, CA 94143 Non-alcoholic fatty liver disease (NAFLD) encompasses a range of liver pathologies from simple steatosis (NAFL) to nonalcoholic steatohepatitis (NASH) and cirrhosis. Impaired mitochondrial b-oxidation has been shown to cause hepatic steatosis in humans and in murine models, and thus may contribute to the pathogenesis and progression of NAFLD. Previously we identified transmembrane protein 55B (TMEM55B), a PI(4,5)P2 phosphatase, as a sterol-regulated gene that modulates cellular and plasma cholesterol levels and impacts lysosome position and function. Considering the emerging role of the lysosome in lipid metabolism and maintenance of mitochondrial function, we investigated the effect of knockdown of TMEM55B on mitochondrial fatty acid oxidation and NAFLD onset and progression to NASH. Treatment of HepG2 cells with siRNA targeting TMEM55B (siTMEM55B) resulted in a 50% reduction in the endogenous mitochondrial oxygen consumption rate (OCR) compared to a scrambled control. Addition of palmitic acid significantly increased OCR by 32% in control (p

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