There is plenty of evidence that Type II (non-insulindependent) diabetes mellitusis a disease with a strong genetic predisposition [1±3]. In Finland, the estimated lifetime relative risk (l) of developing diabetes for a sibling to a person with Type II diabetes is about three [4]. This value decreases with age suggesting that environmental factors become more important with increasing age. Obesity and physical inactivity are the most important triggers of the disease. Several twin studies have provided unequivocal support for the genetic nature of the adult-onset type of diabetes, i. Abstract Aims/hypothesis. To estimate the heritability of insulin sensitivity and insulin secretion, both of which are considered to contribute to the development of Type II (non-insulin-dependent) diabetes mellitus. Methods. Intraclass correlation coefficients and heritability estimates for insulin sensitivity (euglycaemic clamp) as well as first-phase and late-phase insulin secretion (intravenous glucose tolerance test) were calculated in 21 monozygotic and 20 dizygotic twin pairs of the same sex between 54 and 72 years of age. Results. Intrapair correlations for all traits were consistently higher in monozygotic than in dizygotic pairs. Insulin secretion correlated significantly only between monozygotic (first-phase r = 0.55; p = 0.003 and late-phase r = 0.66; p < 0.001) twins giving heritability estimates of 0.55 and 0.58, respectively. Insulinstimulated glucose uptake showed a more modest correlation between monozygotic twins (r = 0.46; p = 0.015). The heritability estimate was 0.37. The heritability estimate for waist-to-hip ratio was 0.76 in female and 0.70 in male twins. Conclusion/interpretation. Genetic variability seems to contribute to the variance of insulin sensitivity as well as of insulin secretion. In the current study, genetic variance accounted almost 60 % for the variance in glucose-stimulated insulin secretion and almost 40 % for the variance in insulin-stimulated glucose uptake. Our data is also compatible with findings in monogenic forms of diabetes in which genetic defects in insulin secretion play a predominant part in the pathogenesis of hyperglycaemia. [Diabetologia (2000) Corresponding author: M. Lehtovirta, Helsinki University Central Hospital, Department of Medicine, Division of Internal Medicine, PO Box 346, FIN-00 029 HYKS, Finland Abbreviations: MZ, Monozygotic; DZ, dizygotic; MODY, maturity-onset diabetes of the young; WHR, waist-to-hip ratio; FFM, fat-free mass; SBP, systolic blood pressure; DBP, diastolic blood pressure; FPI, first-phase insulin secretion in IVGTT; LPI, late-phase insulin secretion in IVGTT; Intraclass r, intraclass correlation coefficient; h 2 , heritability; A, additive component of variance; C, variance component due to shared environment; D, variance component due to dominance; E, variance component due to non-shared environmental influences.