The effects of Formoterol in preventing adipogenesis and obesity are mediated by PPARγ/C/EBPα axis and AMPK/PGC-1α pathway.

Abstract

Recent work suggests that Formoterol could be involved in the metabolic regulation of adipose tissue. It's unknown whether Formoterol possesses an effect against adipogenesis. Here, we found that Formoterol prevented adipocyte differentiation by reducing lipid accumulation, evidenced by reduced Oil Red O staining, declined intracellular triglyceride level, and downregulation of adipogenic factors (PPAR-γ, C/EBPα, and Glut4) in differentiation medium (MDI) stimulated 3T3-L1 preadipocytes. The administration of Formoterol ameliorated obesity in high fat diet (HFD) fed mice, which was evidenced by decreased body weight and ratio of fat/body weight, reduced adipocyte size, and decreased visceral adipocyte tissue weight. Furthermore, the expression level of adipogenic factors in white adipocyte tissues of HFD-fed mice was greatly repressed by Formoterol. Lastly, thermogenic markers (p-AMPK/AMPK, PGC-1α, and UCP-1) were dramatically upregulated by Formoterol. Collectively, Formoterol prevented adipogenesis and obesity in obese mice by regulating the PPARγ/C/EBPα axis and the AMPK/PGC-1α pathway.