The overall goal of the parent proposal is to assess whether developmental (prenatal or early postnatal) exposure to environmental chemicals may be associated with the development of altered glucose metabolism, decreased insulin sensitivity, metabolic inflexibility, and early clinical signs of metabolic syndrome development in a Faroese birth cohort by age 27-28 years. The present - Revision: analyses suggest may cause gene-environment interactions in regard to environmentally associated type 2 diabetes. The targeted approach is in accordance with Faroese legislation and allows a focus on a curated list of linked genes and environmental chemicals for possible gene- environment interaction. Using genetic laboratory facilities at HSPH and relying on the ongoing parent study, where informed consent includes genetic studies, this Revision will address the question whether heterogeneities of candidate genes may modify the glucose metabolism phenotype as potentially affected by exposures to diabetogenic organohalogen compounds. The results will also contribute to the assessment of genetic impact on individual susceptibility and the use of default uncertainty factors in risk assessment.
Because of the increasing prevalence of type 2 diabetes and metabolic syndrome, the proposed research will examine the possible etiologic role of environmental chemicals that appear to be diabetogenic in experimental studies and epidemiological studies, most of which are cross-sectional. We will extend up to age 27 years our follow-up of a Faroese birth cohort with unusually wide ranges of exposures to suspected chemicals and link prenatal and postnatal exposures to glucose metabolism, metabolic flexibility, and body composition as indicators of early development of type 2 diabetes and metabolic syndrome.
