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Single Nucleotide Polymorphisms of the Peroxisome Proliferator–Activated Receptor- Gene (PPARA) Influence the Conversion From Impaired Glucose Tolerance to Type 2 Diabetes

The STOP-NIDDM Trial

Laura Andrulionyt¹, Teemu Kuulasmaa¹, Jean-Louis Chiasson², Markku Laakso¹ for the STOP-NIDDM Study Group^*

¹ Department of Medicine, University of Kuopio and Kuopio University Hospital, Kuopio, Finland
² Research Centre, Centre Hospitalier de l'Université de Montréal, Hôtel-Dieu, and Department of Medicine, University of Montreal, Quebec, Canada

Address correspondence and reprint requests to Markku Laakso, MD, Academy Professor, Department of Medicine, University of Kuopio and Kuopio University Hospital, 70210 Kuopio, Finland. E-mail: markku.laakso{at}kuh.fi

Abbreviations: IGT, impaired glucose tolerance; LD, linkage disequilibrium; PGC-1, PPAR- coactivator 1; PPAR, peroxisome proliferator–activated receptor; SNP, single nucleotide polymorphism

Peroxisome proliferator–activated receptor (PPAR) , a transcription factor of the nuclear receptor superfamily, regulates fatty acid oxidation. We evaluated the association of single nucleotide polymorphisms (SNPs) of the PPAR- gene (PPARA) with the conversion from impaired glucose tolerance to type 2 diabetes in 767 subjects of the STOP-NIDDM trial in order to investigate the effect of acarbose in comparison with placebo on the prevention of diabetes. In the placebo group, the G (162V) allele of rs1800206 increased the risk for diabetes by 1.9-fold (95% CI 1.05–3.58) and was associated with elevated levels of plasma glucose and insulin. The effect of this allele on the risk of diabetes in the placebo group was enhanced by the simultaneous presence of the risk alleles of the PPAR-2, PPAR- coactivator 1, and hepatic nuclear factor 4 genes (odds ratios 2.2, 2.5, and 3.4, respectively). In the acarbose group, subjects carrying the minor G allele of rs4253776 and the CC genotype of rs4253778 of PPARA had a 1.7- and 2.7-fold increased risk for diabetes. Our data indicate that SNPs of PPARA increase the risk of type 2 diabetes alone and in combination with the SNPs of other genes acting closely with PPAR-.

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