Genes and the Metabolic Syndrome Complex Trait Genetics

The genetic basis of MetS has increasingly been appreciated, especially regarding the development of obesity. In this respect, MetS can be considered to result from the interaction of environmental factors, such as caloric excess and physical inactivity, with genetic susceptibility factors.37-39 While the increased prevalence in MetS in the broader population is undoubtedly related to lifestyle - primarily an imbalance between caloric intake and expenditure - it is likely that genetic factors will also be proven to be important. Given the complexity of MetS phenotype, one approach to parse the relative roles of genetic and nongenetic factors is to study MetS in genetically isolated human subpopulations. For instance, in certain North American aboriginal communities, such as the Oji-Cree of Ontario, the combined prevalence of impaired glucose tolerance and type 2 diabetes is approximately 40%.40 This development has been inextricably linked with the recent doubling of hospitalizations for coronary heart disease among Oji-Cree, despite declining rates in the general Canadian population.41 Among Oji-Cree adults aged 35 and older, 43% had MetS.42 Furthermore, 8.7% of female Oji-Cree adolescents had MetS, as defined by the NCEP Adult Treatment Panel (ATP) III47 criteria. Increased waist girth and depressed HDL cholesterol were the most prevalent individual components in subjects with MetS. Common functional polymorphisms in genes encoding proteins involved in the renin angiotensin system, the G-protein family (GNB3) and components of triglyceride-rich lipoproteins were each significantly associated with MetS in Oji-Cree adults, especially women.43 Such studies suggest that the component of genetic susceptibility in MetS is possibly related to genetic basis of the defining intermediate quantitative traits of obesity, dyslipidemia, dysglycemia, and hypertension.

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