Heritability of body mass index in pre-adolescence, young adulthood and late adulthood

Ogata

Environ Health Prev Med

et al. 2015

Objectives The present study aimed to investigate the association between body mass index (BMI) and uric acid (UA) using the twin study methodology to adjust for genetic factors. Methods The association between BMI and UA was investigated in a cross-sectional study using data from both monozygotic and dizygotic twins registered at the Osaka University Center for Twin Research and the Osaka University Graduate School of Medicine. From January 2011 to March 2014, 422 individuals participated in the health examination. We measured height, weight, age, BMI, lifestyle habits (Breslow's Health Practice Index), serum UA, and serum creatinine. To investigate the association between UA and BMI with adjustment for the clustering of a twin within a pair, individual-level analyses were performed using generalized linear mixed models (GLMMs). To investigate an association with adjustment for genetic and family environmental factors, twin-pair difference values analyses were performed. Results In all analysis, BMI was associated with UA in men and women. Using the GLMMs, standardized regression coefficients were 0. Conclusions The present study shows that BMI was significantly associated with UA, after adjusting for both genetic and familial environment factors in both men and women.

Section: Introductionmentioning

confidence: 99%

The relationship between body mass index and uric acid: a study on Japanese adult twins

Ogata

Environ Health Prev Med

et al. 2015

“…This imbalance can be due to genetic or environmental risk factors, or more likely due to a combination of both, an intertwining of genetics and environment [3]. A general consensus is that about 65% of variation in obesity is genetic [4], and candidate genes include those that control energy expenditure and thermogenesis, such as those encoding mitochondrial uncoupling proteins (UCPs) [5].…”

Section: Introductionmentioning

confidence: 99%

Meta-Analysis Reveals the Association of Common Variants in the Uncoupling Protein (UCP) 1–3 Genes with Body Mass Index Variability

et al. 2014

BackgroundThe relationship between uncoupling protein (UCP) 1–3 polymorphisms and susceptibility to obesity has been investigated in several genetic studies. However, the impact of these polymorphisms on obesity is still under debate, with contradictory results being reported. Until this date, no meta-analysis evaluated the association of UCP polymorphisms with body mass index (BMI) variability. Thus, this paper describe a meta-analysis conducted to evaluate if the -3826A/G (UCP1); -866G/A, Ala55Val and Ins/Del (UCP2) and -55C/T (UCP3) polymorphisms are associated with BMI changes.MethodsA literature search was run to identify all studies that investigated associations between UCP1-3 polymorphisms and BMI. Weighted mean differences (WMD) were calculated for different inheritance models.ResultsFifty-six studies were eligible for inclusion in the meta-analysis. Meta-analysis results showed that UCP2 55Val/Val genotype was associated with increased BMI in Europeans [Random Effect Model (REM) WMD 0.81, 95% CI 0.20, 1.41]. Moreover, the UCP2 Ins allele and UCP3-55T/T genotype were associated with increased BMI in Asians [REM WMD 0.46, 95% CI 0.09, 0.83 and Fixed Effect Model (FEM) WMD 1.63, 95% CI 0.25, 3.01]. However, a decreased BMI mean was observed for the UCP2-866 A allele in Europeans under a dominant model of inheritance (REM WMD −0.18, 95% CI −0.35, −0.01). There was no significant association of the UCP1-3826A/G polymorphism with BMI mean differences.ConclusionsThe meta-analysis detected a significant association between the UCP2-866G/A, Ins/Del, Ala55Val and UCP3-55C/T polymorphisms and BMI mean differences.

“…A growing body of evidence suggests that obesity is about 65% genetic and that gene-environment interactions may confer an even greater susceptibility to obesity [30]. One leading hypotheses is that early environmental influences may induce epigenetic variation at specific loci that result in permanent defects in metabolism and increases in disease risk [31].…”

Section: Discussionmentioning

confidence: 99%

Dietary Regimens Modify Early Onset of Obesity in Mice Haploinsufficient for Rai1

et al. 2014

Smith-Magenis syndrome is a complex genomic disorder in which a majority of individuals are obese by adolescence. While an interstitial deletion of chromosome 17p11.2 is the leading cause, mutation or deletion of the RAI1 gene alone results in most features of the disorder. Previous studies have shown that heterozygous knockout of Rai1 results in an obese phenotype in mice and that Smith-Magenis syndrome mouse models have a significantly reduced fecundity and an altered transmission pattern of the mutant Rai1 allele, complicating large, extended studies in these models. In this study, we show that breeding C57Bl/6J Rai1+/− mice with FVB/NJ to create F1 Rai1+/− offspring in a mixed genetic background ameliorates both fecundity and Rai1 allele transmission phenotypes. These findings suggest that the mixed background provides a more robust platform for breeding and larger phenotypic studies. We also characterized the effect of dietary intake on Rai1+/− mouse growth during adolescent and early adulthood developmental stages. Animals fed a high carbohydrate or a high fat diet gained weight at a significantly faster rate than their wild type littermates. Both high fat and high carbohydrate fed Rai1+/− mice also had an increase in body fat and altered fat distribution patterns. Interestingly, Rai1+/− mice fed different diets did not display altered fasting blood glucose levels. These results suggest that dietary regimens are extremely important for individuals with Smith- Magenis syndrome and that food high in fat and carbohydrates may exacerbate obesity outcomes.