Abstract
BackgroundUncoupling protein 2 (UCP2) gene polymorphisms have been reported as genetic risk factors for obesity and type 2 diabetes mellitus (T2DM). We examined the association of commonly observed UCP2 G(−866)A (rs659366) and Ala55Val (C > T) (rs660339) single nucleotide polymorphisms (SNPs) with obesity, high fasting plasma glucose, and serum lipids in a Balinese population.MethodsA total of 603 participants (278 urban and 325 rural subjects) were recruited from Bali Island, Indonesia. Fasting plasma glucose (FPG), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C) and total cholesterol (TC) were measured. Obesity was determined based on WHO classifications for adult Asians. Participants were genotyped for G(−866)A and Ala55Val polymorphisms of the UCP2 gene.ResultsObesity prevalence was higher in urban subjects (51%) as compared to rural subjects (23%). The genotype, minor allele (MAF), and heterozygosity frequencies were similar between urban and rural subjects for both SNPs. All genotype frequencies were in Hardy-Weinberg equilibrium. A combined analysis of genotypes and environment revealed that the urban subjects carrying the A/A genotype of the G(−866)A SNP have higher BMI than the rural subjects with the same genotype. Since the two SNPs showed strong linkage disequilibrium (D’ = 0.946, r2 = 0.657), a haplotype analysis was performed. We found that the AT haplotype was associated with high BMI only when the urban environment was taken into account.ConclusionsWe have demonstrated the importance of environmental settings in studying the influence of the common UCP2 gene polymorphisms in the development of obesity in a Balinese population.
Highlights
Uncoupling protein 2 (UCP2) gene polymorphisms have been reported as genetic risk factors for obesity and type 2 diabetes mellitus (T2DM)
We aim to examine the association of the UCP2 gene G(−866)A and Ala55Val Single Nucleotide Polymorphism (SNP) with obesity, high Fasting plasma glucose (FPG) and serum lipids in a Balinese population, which has not been characterized for the SNPs, comparing the urban and rural population
We propose that the effect of these changes, reflected by the high prevalence of subjects with obesity, high FPG, and serum lipids disorder, was modulated by UCP2 SNPs
Summary
Uncoupling protein 2 (UCP2) gene polymorphisms have been reported as genetic risk factors for obesity and type 2 diabetes mellitus (T2DM). Obesity and T2DM would eventually develop into metabolic disorders and coronary heart disease (CHD), in particular when accompanied with a high serum lipid level. The rapidly increasing prevalence of obesity and T2DM, as well as a high serum lipid level were markedly noticed in developing countries, proposed to be the result of Obesity and T2DM manifested from a combination of genetic predispositions and unfavorable environmental factors, involving unbalanced energy intake and expenditures for basal metabolic process and physical activity [5,6]. One of the key regulators of energy balance is the uncoupling protein 2 (UCP2), a transporter protein present in the mitochondrial inner membrane (UniProt accession P55851) [7]. UCP2 activity may suppress glucose-stimulated insulin secretion, which is regulated by the ATP/ADP ratio [8,9]
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