title: Effect of atorvastatin on SR-BI expression and HDL-induced cholesterol efflux in adipocytes of hypercholesterolemic rabbits.
abstract: BACKGROUND
  Adipose tissue contains a large amount of cholesterol and performs a buffer function for circulating cholesterol. Scavenger receptor class B type I (SR-BI) might play a significant role in adipocytes cholesterol metabolism through mediation of cholesterol efflux. We evaluated the effect of atorvastatin on SR-BI expression and HDL-induced cholesterol efflux in adipocytes from hypercholesterolemic rabbits.
  
  
  METHODS
  Sixteen rabbits fed with high-cholesterol diet for 8 weeks were randomly divided into 2 groups: (1) maintained on a high cholesterol diet for 6 weeks (n=8); (2) the same cholesterol diet plus atorvastatin (2.5 mg/kg/day) for 6 weeks (n=8). Control group (n=5) 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 SR-BI mRNA expression. Cholesterol efflux rate was determined through measuring release of radioactivity from (3)H-cholesterol prelabeled cells into medium containing high-density lipoprotein (HDL). The direct effect of atorvastatin on SR-BI mRNA expression in primary rabbit adipocytes was assayed.
  
  
  RESULTS
  High-cholesterol diet decreased SR-BI mRNA expression and reduced HDL-induced cholesterol efflux rate in adipocytes. Six weeks of atorvastatin treatment significantly enhanced the cholesterol efflux from adipocytes, which was related to the increased mRNA expression of SR-BI (r=0.58, P<0.05). Adipocytes SR-BI mRNA expression were negatively correlated with the serum total cholesterol levels at the end of the study (r=-0.46, P<0.05). Atorvastatin dose-dependently stimulated SR-BI mRNA expression in cultured adipocytes.
  
  
  CONCLUSIONS
  Atorvastatin can up-regulate SR-BI mRNA expression and promote the HDL-induced cholesterol efflux in adipocytes from hypercholesterolemic rabbits possibly through lowering serum cholesterol levels and directly stimulating SR-BI mRNA expression.
authors.affiliation: Department of Cardiology, The Second Xiangya Hospital of Central South University, middle Ren-Min road No. 86, Changsha, Hunan 410011, PR China.
authors.forename: Shui-Ping
authors.initials: SP
authors.lastname: Zhao
authors.forename: Zhi-Hong
authors.initials: ZH
authors.lastname: Wu
authors.forename: Shao-Cai
authors.initials: SC
authors.lastname: Hong
authors.forename: Hui-Jun
authors.initials: HJ
authors.lastname: Ye
authors.forename: Jie
authors.initials: J
authors.lastname: Wu
mesh_terms: D017667:Adipocytes / Q000187:drug effects* / Q000378:metabolism; D000818:Animals; D000924:Anticholesteremic Agents / Q000494:pharmacology*; D000069059:Atorvastatin; D001692:Biological Transport; D018955:CD36 Antigens / Q000235:genetics*; D002784:Cholesterol / Q000378:metabolism*; D017931:DNA Primers; D006538:Heptanoic Acids / Q000494:pharmacology*; D066298:In Vitro Techniques; D008075:Lipoproteins, HDL / Q000378:metabolism*; D008297:Male; D011758:Pyrroles / Q000494:pharmacology*; D012333:RNA, Messenger / Q000235:genetics; D011817:Rabbits; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D000924:Anticholesteremic Agents; D018955:CD36 Antigens; D017931:DNA Primers; D006538:Heptanoic Acids; D008075:Lipoproteins, HDL; D011758:Pyrroles; D012333:RNA, Messenger; D002784:Cholesterol; D000069059:Atorvastatin