| beta3AR Trp64Arg and GLUT1 polymorphisms are common in several ethnic groups. beta3AR is important for mediating the stimulation of lipolysis by catecholamine. Recent studies have suggested that a missense Trp64Arg mutation in the beta3AR gene was involved in visceral obesity and insulin resistance. GLUT1 is responsible for the general basal glucose transport. Previous studies suggested that GLUT1 XbaI polymorphism was associated with IR.;Objective. To explore the relative contribution of genetic and environmental effects to insulin sensitivity (1/IR), and investigate the influences of beta3AR Trp64Arg and GLUT1 XbaI polymorphisms on IR.;Results. The AE-model fitted the data best. The influence of age on overall model was not significant (chi2 = 1.851, P = 0.604), but the heritability of insulin sensitivity decreased with age and this decline was mainly due to a dramatical decrease in additive genetic component. The heritability of insulin sensitivity based on AE model was 0.35 in male and 0.46 in female, respectively. The genotypic frequencies of Trp/Trp, Trp/Arg and Arg/Arg were 71.5%, 26.7% and 1.7%. Those who carried Trp64Arg variant had trends towards lower insulin sensitivity compared to the one who carried normal genotype, but had no significance (P = 0.145). BMI showed to be positively correlated with LogHOMA. We found no significant association between the Trp64Arg variant and BMI. The three genotypic frequencies of GLUT1 (wildtype, heterozygote and variant homozygote) were 64.0%, 33.7% and 2.3%. No significant association between the GLUT1 XbaI polymorphism and LogHOMA was found in the present study.;Conclusion. 35% of the variance of insulin sensitivity was due to additive effects in male and 46% was due to additive effects in female. The presence of the Arg64 allele in beta3AR gene may predispose patients to insulin resistance. Further study with larger sample size may help to confirm the results. GLUTI Xbal polymorphism is unlikely to play a significant role in IR. (Abstract shortened by UMI.). |
