In conclusion, our results suggest that the -866 AA genotype and A allele of the UCP2 gene is associated with obesity and A allele associated with hyperinsulinemia in obese subjects.
To assess functional correlates of -866G>A, we compared uncoupling protein 2 (UCP2) expression in the skeletal muscle of obese participants by genotype and compared the activity of UCP2 luciferase promoters with -866G and -866A alleles.
Uncoupling Protein 2 (UCP2) is an attractive candidate to screen for NTD risk because of its possible role in obesity as well as energy metabolism, type-2 diabetes, and the regulation of reactive oxygen species.
Genetic variation in the UCP2-UCP3 gene cluster may act as a modifier increasing serum lipid levels and indices of abdominal obesity, and may thereby also contribute to the metabolic aberrations observed in obesity and type 2 diabetes.
The aim of this study was to examine whether there is an association between the UCP2/UCP3 locus and the obesity in the Japanese population when using a single nucleotide polymorphism (SNP)-based and haplotype-based case-control study with gender-specific analysis.
This review summarizes data supporting the roles of UCP2 and UCP3 in energy dissipation, as well as the genetic variety association with fat metabolism, obesity and diabetes in humans.
Our results suggest that subjects with a 45bp insertion allele of UCP2+3474 ins/del might have a higher risk of developing obesity, although the biological effects of this variant are not completely known.
Our findings indicate that the uncoupling protein 2 gene -866G/A polymorphism may increase the risks of central obesity and metabolic syndrome, with greater effects on Asian men.
In this study, we investigated the effects of genetic variation in UCP2 on type 2 diabetes and obesity, as well as on metabolic phenotypes related to these diseases, in Pima Indians.
Our results suggest that the LEP and UCP2/UCP3 genes are unlikely to have a substantial effect on variation in obesity phenotypes in this particular US Caucasian population.
The mitochondrial uncoupling proteins (UCP-2 and UCP-3), which have been suggested to be involved in the development of obesity by controlling the energy expenditure (EE), were studied in 22 healthy first-degree relatives (FDRs) of patients with type 2 diabetes and 13 body mass index (BMI)- and age-matched healthy control subjects.
A common -866G/A promoter polymorphism that has been associated with obesity and beta-cell function may also affect UCP2 gene expression in cells of the arterial wall.
Obesity risk among carriers of the UCP2 insertion allele was slightly higher than among non-carriers (unadjusted odds ratio, 1.42; 95% confidence interval, 0.90 to 2.23); however, when the model was adjusted for sex, age, physical activity, and sedentary lifestyle (hours spent sitting down), a statistically significant odds ratio of obesity (1.94; 95% confidence interval, 1.14 to 3.30; P = 0.01) for carriers of the UCP2 insertion allele was found.
To clarify the contribution of this polymorphism to obesity and related conditions, we studied the association of the -866 G/A polymorphism of the UCP2 gene with obesity, hypertension and type 2 diabetes mellitus.