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Mitochondrial ACSS1-K-635 acetylation mimic knock-in mice exhibit altered lipid metabolism, hepatic cell senescence, and acute non-alcoholic fatty liver [2ndSet_analysis]

ABSTRACT: We generated an ACSS1-acetylation (Ac) mimic mouse, where lysine 635 was mutated to glutamine (K635Q). Male Acss1K635Q/K635Q mice were smaller with higher metabolic rate and blood acetate, and decreased liver/serum ATP and lactate levels. After a 48-hour fast, Acss1K635Q/K635Q mice presented hypothermia and liver aberrations, including enlargement, discoloration, lipid droplet accumulation, and microsteatosis – consistent with nonalcoholic fatty liver disease (NAFLD). RNAseq analysis suggested dysregulation of fatty acid metabolism, cellular senescence, and hepatic steatosis networks, consistent with NAFLD

ORGANISM(S): Mus musculus

PROVIDER: GSE260582 | GEO | 2024/04/12

REPOSITORIES: GEO

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Mitochondrial ACSS1-K-635 acetylation mimic knock-in mice exhibit altered lipid metabolism, hepatic cell senescence, and acute non-alcoholic fatty liver [1stSet_analysis]

Project description:We generated an ACSS1-acetylation (Ac) mimic mouse, where lysine 635 was mutated to glutamine (K635Q). Male Acss1K635Q/K635Q mice were smaller with higher metabolic rate and blood acetate, and decreased liver/serum ATP and lactate levels. After a 48-hour fast, Acss1K635Q/K635Q mice presented hypothermia and liver aberrations, including enlargement, discoloration, lipid droplet accumulation, and microsteatosis – consistent with nonalcoholic fatty liver disease (NAFLD). RNAseq analysis suggested dysregulation of fatty acid metabolism, cellular senescence, and hepatic steatosis networks, consistent with NAFLD.

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