Brown University

Aspartate-β-hydroxylase suppresses nonalcoholic fatty liver progression by regulating AMPK phosphorylation and SREBP-1c expression.

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Abstract:
NAFLD affects more than one-quarter of adults worldwide with 60% in diabetic patients and 90% in obese people. Aspartate beta-hydroxylase (ASPH), an alpha-ketoglutarate dependent enzyme hydroxylase that has been linked to hepatocellular carcinoma, recently shown to suppress NAFLD progression by regulating AMPK phosphorylation and SREBP1c expression, which are important regulators in lipid and glucose metabolism. B6 mice have been successfully genetically modified with human ASPH gene. Using those transgenic mice, we demonstrated that human ASPH overexpression decreases liver weight in mice fed with a high-fat diet. Moreover; western blot shows that overexpression of ASPH in mice fed with high-fat diet play a role in lipid and glucose metabolism by activating AMPK phosphorylation and suppressing SREBP1c expression. ASPH overexpression reduces hepatic lipid accumulation as shown in the histology staining and lipid analysis. Our study indicates the potential of ASPH as a therapeutic target in NAFLD.
Notes:
Thesis (Sc. M.)--Brown University, 2020

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Citation

Mulla, Joud Issam, "Aspartate-β-hydroxylase suppresses nonalcoholic fatty liver progression by regulating AMPK phosphorylation and SREBP-1c expression." (2020). Molecular Pharmacology, Physiology, and Biotechnology Theses and Dissertations. Brown Digital Repository. Brown University Library. https://doi.org/10.26300/xmhw-ve62

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