Effect of niacin on LXRα and PPARγ expression and HDL-induced cholesterol efflux in adipocytes of hypercholesterolemic rabbits

Background Adipose tissue contains a large amount of cholesterol and performs a buffer function for circulating cholesterol. Liver X receptors (LXR) α and peroxisome proliferator-activated receptor γ (PPARγ) might play a significant role in adipocyte cholesterol metabolism through mediation of cholesterol efflux. The aim of this study was to evaluate the effect of niacin on LXRα and PPARγ expression and HDL-induced cholesterol efflux in adipocytes from hypercholesterolemic rabbits. Methods Twelve rabbits fed with high-cholesterol diet for 8 weeks were randomly divided into two groups: (1) high cholesterol group (n = 6): maintained high cholesterol diet for 6 weeks; (2) niacin group (n = 6): the same cholesterol diet plus niacin (200 mg/kg/d) for 6 weeks. Control group (n = 6) was fed with normal diet for 14 weeks. Subcutaneous adipose was collected for adipocyte culture. Reverse transcription polymerase chain reaction (RT-PCR) was used to evaluate adipocytes LXRα mRNA expressions. Cholesterol efflux rate was determined through measuring release of radioactivity from 3H-cholesterol prelabeled cells into medium containing high-density lipoprotein (HDL). The direct effect of niacin on LXRα and PPARγ mRNA expression in primary rabbit adipocytes was assayed. Results High cholesterol diet resulted in decreased LXRα mRNA expressions and reduced HDL-induced cholesterol efflux rate in adipocytes. Six weeks of niacin treatment significantly enhanced the cholesterol efflux from adipocytes, which was related to the increased mRNA expressions of LXRα (r = 0.71, P < 0.05). In in vitro study, niacin dose-dependently stimulated LXRα and PPARγ mRNA expression in cultured adipocytes. And various doses of niacin-induced cholesterol efflux was positive correlation with LXRα and PPARγ mRNA expression (r = 0.83 P < 0.01; r = 0.76 P < 0.05; respectively). Conclusion Niacin can up-regulate LXRα and PPARγ mRNA expression and promote the HDL-induced cholesterol efflux in adipocytes from hypercholesterolemic rabbits.