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Genetic and Environmental Effects on Fasting and Postchallenge Plasma Glucose and Serum Insulin Values in Finnish Twins
Author(s) -
Shūichi Katoh,
Mikko Lehtovirta,
Jaakko Kaprio,
Valma Harjutsalo,
Markku Koskenvuo,
Johan G. Eriksson,
Naoko Tajima,
Jaakko Tuomilehto
Publication year - 2005
Publication title -
the journal of clinical endocrinology and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.206
H-Index - 353
eISSN - 1945-7197
pISSN - 0021-972X
DOI - 10.1210/jc.2004-2471
Subject(s) - endocrinology , medicine , insulin , waist , insulin resistance , intraclass correlation , genetic correlation , genetic variation , impaired glucose tolerance , twin study , biology , heritability , body mass index , genetics , clinical psychology , gene , psychometrics
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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