Short chain fatty acids increase fat oxidation and promote browning through 03-adrenergic receptor/AMP-activated protein kinase ? signaling pathway in 3T3-L1 adipocytes

To investigate the molecular mechanism of short chain fatty acids (SCFAs) on promoting fatty acid 0-oxidation and browning in 3T3-L1 adipocytes. SCFAs significantly reduced lipid accumulation in 3T3-L1 adipocytes. In addition, via increasing the expression of Tfam and Nrf1, SCFAs enhanced mitochondrial biogenesis. According to the results of qPCR analysis, the expression levels of fatty acid 0-oxidation genes (PPAR alpha, CPT1 alpha, ACOX1) were up-regulated by SCFAs. Moreover, SCFAs treatment increased the genes and proteins expression of brown adipocyte-specific factors such as PRDM16, PGC-1 alpha, and UCP-1, as well as up-regulated the genes expression of beige adipocytes markers (Tmem26, Tbx1, CD137, and Cited1). Furthermore, the effects of 03-AR and AMPK antagonist were reversed by SCFAs. In conclusion, SCFAs promote fat 0-oxidation and browning of adipocytes through 03-AR/AMPK alpha signaling pathway, thereby reducing fat accumulation in 3T3-L1 adipocytes. Therefore, SCFAs may be a helpful supplement to combat obesity.

Automated summary

Short chain fatty acids (SCFAs) promote fatty acid 0-oxidation and browning in 3T3-L1 adipocytes by regulating the 03-AR/AMPKα signaling pathway. SCFAs reduce lipid accumulation and enhance mitochondrial biogenesis. They also up-regulate the expression of fatty acid 0-oxidation genes and brown adipocyte-specific factors.