Recombinant globular adiponectin inhibits lipid deposition by p38 MAPK/ATF-2 and TOR/p70 S6 kinase pathways in chicken adipocytes.

Adiponectin plays a fundamental role in lipid and carbohydrate metabolism. However, its role in adipocyte differentiation remains controversial. To investigate the effect of gAd on lipid deposition in chicken adipocytes and its related signaling pathways, 200 μg/mL recombinant globular adiponectin, isoproterenol, SB253580, leucine, and rapamycin were used to treat chicken adipocytes. Results demonstrated that gAd increased the expression of endogenous adiponectin and AdipoR1 (P < 0.01); gAd inhibited triglyceride (TG) accumulation in chicken adipocyte and increased the release of free fatty acids (FFA) in medium; gAd decreased the expression of adipogenic marker genes CCAAT/enhancer binding protein alpha (C/EBPα) and fatty acid synthase (FAS), while activating the expression of lipolytic marker gene adipose triglyceride lipase (ATGL) (P < 0.01). Meanwhile, gAd activated the phosphorylation levels of p38 mitogen-activated protein kinase (p38 MAPK) and activating transcription factor 2 (ATF-2), and suppressed the phosphorylation levels of rapamycin (TOR) and p70 S6 Kinase (P < 0.01). In conclusion, the results demonstrate that gAd has an ability to inhibit lipids deposition in chicken adipocyte, which depends on the p38 MAPK/ATF-2 and TOR/p70 S6 Kinase pathways.

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