Soat2 ties cholesterol metabolism to β-oxidation and glucose tolerance in male mice.
Camilla PramfalkOsman AhmedMatteo PedrelliMirko E MinnitiSerge LuquetRaphaël Gp DenisMaria OlinJennifer HärdfeldtLise-Lotte VedinKnut R SteffensenMikael RydénLeanne HodsonMats ErikssonPaolo PariniPublished in: Journal of internal medicine (2022)
Our data demonstrate that ACAT2-generated cholesteryl esters negatively affect the metabolic control by retaining TG in the liver and that genetic inhibition of Soat2 improves liver steatosis via partitioning of lipids into secretory (VLDL-TG) and oxidative (fatty acids) pathways.