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  • 1
    Electronic Resource
    Electronic Resource
    Insulin secretion and insulin sensitivity in diabetic subgroups: studies in the prediabetic and diabetic state (2000)
    Springer
    Diabetologia 43 (2000), S. 1476-1483 
    Details
    ISSN: 1432-0428
    Keywords: Keywords LADA ; MODY ; Type II diabetes ; IGT ; insulin secretion ; insulin sensitivity.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. To evaluate insulin sensitivity and insulin secretion in prediabetic and diabetic subjects with mutations in MODY1 (HNF-4α) and MODY3 (HNF-1α) genes, in subjects with GAD antibodies, latent autoimmune diabetes in adults and in subjects with the common form of Type II (non-insulin-dependent) diabetes mellitus. Methods. Insulin secretion was measured as the incremental 30-min insulin (I30) and insulin glucose ratio (I:G30) during OGTT whereas insulin sensitivity was measured as the insulin sensitivity index during OGTT in 131 carriers of MODY mutations [NGT = 38, IFG/IGT = 21, diabetes mellitus (DM) = 72], in 293 subjects with GADA (NGT = 47, IFG/IGT = 29, DM = 217) and in 2961 subjects with a family history of the common form of Type II diabetes but without MODY mutations or GADA (NGT = 1360, IFG/IGT = 857, DM = 744). A subgroup of the subjects underwent a euglycaemic clamp (n = 210) and intravenous glucose tolerance test (n = 337) for the estimation of insulin sensitivity and first-phase insulin secretion. Results. Non-diabetic subjects with MODY mutations had pronounced impaired insulin secretion (I30, I:G30) compared with the two other groups (p = 0.005). Normal or non-diabetic glucose tolerance was maintained by enhanced insulin sensitivity compared with the other two groups (p 〈 0.05 and p 〈 0.005). In contrast to patients with Type II diabetes and with adult latent autoimmune diabetes, MODY patients showed only a modest deterioration in insulin sensitivity at onset of diabetes. The 2-h glucose values inversely correlated with insulin sensitivity in subjects with GADA (r = –0.447, p 〈 0.001) and subjects from Type II diabetic families (r = –0.426, p 〈 0.001), whereas no such relation was observed in subjects with MODY mutations (r = 0.151, p = NS). There were no statistically significant differences in insulin secretion or insulin sensitivity between subjects with GADA or subjects with a family history of Type II diabetes, either at the NGT or the IFG/IGT stage. Conclusion/interpretation. Glucose-tolerant carriers of MODY mutations are characterised by a severe impairment in insulin secretion. Enhanced insulin sensitivity is the most likely explanation for the normal glucose tolerance. Whereas subjects with positive GADA or Type II diabetes have impaired insulin sensitivity with increasing glucose concentrations, MODY mutation carriers seem to be protected from the effect of glucose toxicity. [Diabetologia (2000) 43: 1476–1483]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051558
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  • 2
    Electronic Resource
    Electronic Resource
    Insulin sensitivity and insulin secretion in monozygotic and dizygotic twins (2000)
    Springer
    Diabetologia 43 (2000), S. 285-293 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Twins, monozygotic, dizygotic, heritability, insulin, insulin resistance.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: 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. Insulin-stimulated 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) 43: 285–293]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050046
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  • 3
    Electronic Resource
    Electronic Resource
    Determinants of postabsorptive endogenous glucose output in non-diabetic subjects (2000)
    Springer
    Diabetologia 43 (2000), S. 1266-1272 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Endogenous glucose production, insulin resistance, insulin.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aim/hypothesis. To gain insight into the physiologic determinants of postabsorptive endogenous glucose output (EGO) in humans.¶Methods. We analysed the data of 344 non-diabetic subjects (212 men and 132 women) with a wide range of age (18–85 years) and body mass index (15–55 kg/m2) who participated in the European Group for the Study of Insulin Resistance (EGIR) project. Whole-body endogenous glucose output was measured by tracer ([3H]glucose) dilution at steady-state, peripheral insulin sensitivity (Ñ glucose clearance/Ñ insulin) was measured by the euglycaemic insulin (7 pmol × min–1× kg–1) clamp technique.¶Results. Whole-body endogenous glucose output showed a large variability (mean = 768 ± 202 μmol · min–1, range 209–1512) and was strongly related to lean body mass (r = 0.63, p 〈 0.0001). This association entirely explained the endogenous glucose output being higher in men than in women (827 ± 189 vs 674 × 187 μmol × min–1, p 〈 0.0001), its relation to body mass (+ 10 ± 2 per unit of body mass index, p 〈 0.0001) and its trend to decline with age (–1.1 ± 0.7 μmol · min–1 per year, p = 0.10). Although inversely related to one another (r = –0.41, p 〈 0.0001), peripheral insulin sensitivity and fasting plasma insulin were both independently associated with endogenous glucose output in an inverse fashion (with partial r's of 0.19 and 0.21, respectively, after adjusting for lean body mass and centre, p 〈 0.0001 for both).¶Conclusion/interpretation. Among non-diabetic subjects in the postabsorptive condition, total body endogenous glucose output variability is wide and is largely explained by the amount of lean mass; this, in turn, explains differences in total endogenous glucose output due to sex, obesity and age. Independently of the amount of lean mass, peripheral insulin resistance is associated with a higher endogenous glucose output independently of fasting plasma insulin concentration, suggesting coupled regulation of insulin action in peripheral tissues and the liver. [Diabetologia (2000) 43: 1266–1272]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051522
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    Paper (German National Licenses)
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