title: Effects of PPARγ and RBP4 gene variants on metabolic syndrome in HIV-infected patients with anti-retroviral therapy.
abstract: BACKGROUND
  PPARγ and RBP4 are known to regulate lipid and glucose metabolism and insulin resistance. The influences of PPARγ (C1431T and Pro12Ala) and RBP4 (-803GA) polymorphisms on metabolic syndrome in HIV-infected patients receiving anti-retroviral therapy were examined in this study.
  
  
  METHODS
  A cross-sectional study of HIV-1 infected adults with antiretroviral therapy for more than one year in the National Cheng Kung University Hospital was conducted. The gene polymorphisms were determined by quantitative PCR.
  
  
  RESULTS
  Ninety-one patients were included in the study. Eighty-two (90.1%) patients were males with a mean age of 44.4 years. For the C1431T polymorphism in PPARγ, while patients with the T allele (48.4%) had trends toward lower rate of hypertriglyceridemia, the borderline significance together with insignificant power did not support the protective effect of the T allele against development of hypertriglyceridemia. For the Pro12Ala polymorphism in PPARγ, although patients with the Pro/Ala genotype (8.8%) had a higher level of serum LDL (138.0 vs. 111.5 mg/dl, P = 0.04) and trends toward higher rates of hypercholesterolemia and serum LDL>110 mg/dl, these variables were found to be independent of the Pro/Ala genotype in the multivariate analysis. For the -803GA polymorphism in RBP4, patients with the A allele (23.1%) more often had insulin resistance (HOMA>3.8; 33.3 vs. 8.7%, P = 0.01) and more often received anti-hypoglycemic drugs (14.3 vs. 1.4%, P = 0.04). The detrimental effect of the A allele in RBP4 -803GA polymorphism on development of insulin resistance was supported by the multivariate analysis adjusting for covariates.
  
  
  CONCLUSIONS
  The impacts of PPARγ C1431T and Pro12Ala polymorphisms on metabolism in HIV-infected patients are not significant. RBP4 -803GA polymorphism has increased risk of insulin resistance in HIV-infected patients with anti-retroviral therapy.
authors.affiliation: Institute of Clinical Medicine, National Cheng Kung University, Tainan, Taiwan.
authors.forename: Yuan-Pin
authors.initials: YP
authors.lastname: Hung
authors.forename: Nan-Yao
authors.initials: NY
authors.lastname: Lee
authors.forename: Sheng-Hsiang
authors.initials: SH
authors.lastname: Lin
authors.forename: Ho-Ching
authors.initials: HC
authors.lastname: Chang
authors.forename: Chi-Jung
authors.initials: CJ
authors.lastname: Wu
authors.forename: Chia-Ming
authors.initials: CM
authors.lastname: Chang
authors.forename: Po-Lin
authors.initials: PL
authors.lastname: Chen
authors.forename: Hsiao-Ju
authors.initials: HJ
authors.lastname: Lin
authors.forename: Yi-Hui
authors.initials: YH
authors.lastname: Wu
authors.forename: Pei-Jane
authors.initials: PJ
authors.lastname: Tsai
authors.forename: Yau-Sheng
authors.initials: YS
authors.lastname: Tsai
authors.forename: Wen-Chien
authors.initials: WC
authors.lastname: Ko
mesh_terms: D000328:Adult; D000483:Alleles; D023241:Antiretroviral Therapy, Highly Active; D003430:Cross-Sectional Studies; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D015658:HIV Infections / Q000150:complications / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism; D015497:HIV-1 / Q000235:genetics; D006801:Humans; D007333:Insulin Resistance / Q000235:genetics; D008297:Male; D024821:Metabolic Syndrome / Q000150:complications / Q000188:drug therapy / Q000378:metabolism; D008875:Middle Aged; D047495:PPAR gamma / Q000235:genetics*; D020641:Polymorphism, Single Nucleotide; D054839:Retinol-Binding Proteins, Plasma / Q000235:genetics*; D055815:Young Adult
chemical_list: D047495:PPAR gamma; C101326:RBP4 protein, human; D054839:Retinol-Binding Proteins, Plasma