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Diabetes and Genetic Epidemiology Unit (S.K., V.H., J.E., J.T.), Department of Epidemiology and Health Promotion, and Department of Mental Health and Alcohol Research (J.K.), National Public Health Institute, FIN-00300 Helsinki, Finland; Division of Diabetes and Endocrinology (S.K., N.T.), Department of Internal Medicine, Jikei University School of Medicine, 105-8461 Tokyo, Japan; Department of Medicine (M.L.), Helsinki University Hospital, FIN-00029 HUS Helsinki, Finland; Department of Public Health (J.K., J.T., S.K., J.E.), University of Helsinki, Helsinki FI-00014, Finland; Department of Public Health (M.K.), University of Turku, FI-20520 Turku, Finland; and South Ostrobotnia Central Hospital (J.T.), FIN-60101 Seinäjoki, Finland
Address all correspondence and requests for reprints to: Jaakko Kaprio, M.D., Ph.D., Department of Public Health, P.O. Box 41 (Mannerheimintie 172), University of Helsinki, FIN-00014 Helsinki, Finland. E-mail: jaakko.kaprio{at}helsinki.fi.
The aim of this study was to evaluate genetic and environmental effects on plasma glucose, insulin secretion, and resistance in Finnish twins. Altogether 151 randomly selected twin pairs were examined by the oral glucose tolerance test; 66 twin pairs were monozygotic and 85 like-sexed dizygotic. We estimated the intraclass correlation coefficients and variance components of genetic and environmental effects on waist circumference, plasma glucose, and serum insulin. For fasting insulin, the proportion of total variation accounted for by additive genetic effects (A) and nonshared environmental effects (E) were 43 and 57%, respectively. As to postchallenge insulin and waist circumference, A effects were stronger in female twins (51 and 70%, respectively) than male twins in whom no significant evidence for genetic variance was found. Of the variation in fasting glucose, A and E effects accounted for 45 and 55%, respectively. Of the variation in postchallenge glucose, E effects had a greater role (65%), compared with A effects (35%); A effects on pre- and postchallenge insulin levels were highly correlated (genetic correlation coefficient = 0.81). In conclusion, additive genetic effects are important for the insulin secretion, whereas nonshared environmental effects contribute strongly to peripheral insulin resistance.
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