Resveratrol (RES) is one of the best-known bioactive polyphenols that has received much attention in recent years because of its importance to anti-obesity. However, the exact mechanism underlying this effect and whether it can improve lipid metabolism by regulating the long-chain noncoding RNA (lncRNA) remains unclear. In this study, 24 healthy crossbred castrated boars were fed a basal diet (control) and a basal diet supplemented with 200 mg, 400 mg or 600 mg RES per Kilogram (kg) of feed for 41 d, respectively. We found that 400 mg/kg and 600 mg/kg RES-supplemented diet did not affect growth rate, but reduced significantly subcutaneous adipose thickness, carcass fat rate, greater dramatically the serum concentration of adiponectin and high-density lipoprotein in pigs. Further, we verified that RES could inhibit the formation and accumulation of lipid droplets by AdipoQ-AdipoR1-AMPKα and AdipoQ-AdipoR2-PPARα signal pathway in vivo and vitro (3T3-L1 preadipocytes). Transcriptome analyses found that 5 differently expressed (DE) lncRNAs and 77 mRNAs in subcutaneous adipose between control group and 400 mg/kg RES group, which mainly involved in "adipocytokine signaling pathway," "Wnt signaling pathway," "PI3K-Akt signaling pathway" and "MAPK signaling pathway." In conclusion, RES can inhibit the formation and accumulation of lipid droplets through AdipoQ signal pathway and lipid metabolism-related lncRNAs. Our results provide a new insight on the molecular mechanism of RES as a nutritional agents to the prevention and treatment for obesity.
Keyphrases
- signaling pathway
- pi k akt
- insulin resistance
- weight loss
- fatty acid
- cell proliferation
- metabolic syndrome
- induced apoptosis
- epithelial mesenchymal transition
- high density
- cell cycle arrest
- adipose tissue
- physical activity
- skeletal muscle
- stem cells
- network analysis
- high fat diet induced
- cell death
- weight gain
- gene expression
- genome wide
- single cell
- combination therapy
- dna methylation
- long noncoding rna
- molecular dynamics
- transcription factor