The sphingosine-1-phosphate receptor 2 S1PR2 mediates chronic glucocorticoid exposure-induced hepatic steatosis and hypertriglyceridemia.

ABSTRACT: Glucocorticoids are potent anti-inflammatory agents that are frequently used to treat inflammatory and autoimmune diseases. Chronic glucocorticoid treatment, however, causes unwanted adverse effects such as hypertriglyceridemia and hepatic steatosis. Here we showed that reducing the expression of sphingosine-1-phosphate receptor 2 (S1PR2) in mice liver reduced chronic glucocorticoid exposure induced triglyceride accumulation in the liver and the plasma. Chronic glucocorticoid treatment increased the recruitment of sterol regulatory element-binding protein 1c (Srebp1c) to the sterol regulatory element of mouse fatty acid synthase (Fasn) gene. This response was attenuated in hepatic S1PR2 knockdown mice. Chronic glucocorticoid treatment also increased the recruitment of carbohydrate response

SUBMITTER: Chang M 

PROVIDER: S-EPMC12274751 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature