The transcription factor RXRA regulates lipid metabolism in duck myoblasts by the CD36 network

Abstract

Lipid metabolism is a highly complex metabolic process regulated at multiple levels. RXRA is a well-characterized factor that regulates lipid metabolism. To explore the function and mechanism of the transcription factor RXRA in myoblasts, and to further explore the key factors that RXRA regulates the target gene CD36 signaling network to regulate lipid metabolism. We found that the transcription factor RXRA inhibited the accumulation of triglycerides (TGs), cholesterol (CHOL) and non-esterified fatty acids (NEFA) in CS2 cells by regulating CD36 as well as the fatty acid beta oxidation pathway. CD36 functions similar to RXRA in myoblasts. CD36 overexpression reduced the levels of TGs, CHOL, NEFAs and saturated fatty acids (SFAs) in these cells, while CD36 knockout increased the levels of TGs, CHOL, NEFAs, SFAs and monounsaturated fatty acids (MUPAs) in these cells. GRB2, MAP1B, SLC38A1, SLC4A7, NCOA3, PKIA, MOB2, SAA2 and RXRA are involved in the CD36 promotion of lipid efflux through lipid metabolism, endocytosis and amino acid metabolism. Considering these results, we propose that RXRA regulates lipid metabolism in myoblasts by regulating the CD36 signaling network.