Article

The influence of exposure to maternal diabetes in utero on the rate of decline in β-cell function among youth with diabetes.

Journal of pediatric endocrinology & metabolism: JPEM (Impact Factor: 0.71). 05/2013; DOI: 10.1515/jpem-2012-0385
Source: PubMed

ABSTRACT Abstract We explored the influence of exposure to maternal diabetes in utero on β cell decline measured by fasting C-peptide (FCP) among 1079 youth <20 years with diabetes, including 941 with type 1 and 138 with type 2 diabetes. Youths exposed to maternal diabetes had FCP levels that were 17% lower among youth with type 2 diabetes [95% confidence interval (CI): -34%, +6%] and 15% higher among youth with type 1 diabetes (95%CI: -14%, +55%) than their unexposed counterparts, although differences were not statistically significant (p=0.13 and p=0.35, respectively). Exposure to maternal diabetes was not associated with FCP decline in youth with type 2 (p=0.16) or type 1 diabetes (p=0.90); nor was the effect of in utero exposure on FCP modified by diabetes type. Findings suggest that exposure to maternal diabetes in utero may not be an important determinant of short-term β-cell function decline in youth with type 1 or type 2 diabetes.

0 Bookmarks
 · 
61 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: To test the hypothesis that long-term postnatal development may be modified by metabolic experiences in utero. We enrolled offspring of women with pregestational diabetes (this included insulin-dependent diabetes mellitus [IDDM] and non-insulin-dependent diabetes mellitus [NIDDM]) and gestational diabetes in a prospective study from 1977 through 1983. Fetal beta-cell function was assessed by measurement of amniotic fluid insulin (AFI) at 32-38 weeks gestation. Postnatally, plasma glucose and insulin were measured yearly from 1.5 years of age after fasting and 2 h after 1.75 g/kg oral glucose. Control subjects had a single oral glucose challenge at 10-16 years. In offspring of diabetic mothers, the prevalence of impaired glucose tolerance (IGT) (2-h glucose concentration > 7.8 mmol/l) was: 1.2% at < 5 years, 5.4% at 5-9 years, and 19.3% at 10-16 years. The 88 offspring of diabetic mothers (12.3 +/- 1.7 years), when compared with 80 control subjects of the same age and pubertal stage, had higher 2-h glucose (6.8 +/- 1.4 vs. 5.7 +/- 0.9 mmol/l, P < 0.001) and insulin (660 +/- 720 vs. 455 +/- 285 pmol/l, P < 0.03) concentrations. The 17 subjects with IGT at > 10 years of age (9 boys and 8 girls) include one girl with NIDDM. IGT was not associated with the etiology of the mother's diabetes (gestational versus pregestational) or macrosomia at birth. IGT was found in only 3.7% (1 of 27) of adolescents whose AFI was normal ( < or = 100 pmol/l) and 33.3% (12 of 36) of those with elevated AFI (P < 0.001). Although most of the children with IGT are obese, AFI and obesity are independently associated with IGT by multiple logistic analysis. In confirmation of our original hypothesis, IGT in the offspring is a long-term complication of maternal diabetes. Excessive insulin secretion in utero, as assessed by AFI concentration, is a strong predictor of IGT in childhood.
    Diabetes Care 06/1995; 18(5):611-7. · 8.57 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Adult offspring of diabetic rat mothers display a disturbed glucose tolerance and gestational diabetes. The amount of endocrine pancreas and of B-cells is largely sufficient in these non-pregnant and pregnant youngsters. The present work aims a morphometric evaluation of B-cell activity in adult youngsters from control, mildly and severely diabetic mothers, in basal condition and in their adaptation to pregnancy. B-cells are divided, on basis of the ultrastructural morphology of their organelles, in dark non-activated B-cells and pale activated B-cells. These data are related to the concepts of functional B-cell heterogeneity and dose-dependent recruitment of pancreatic B-cells on stimulation. The recruitment of B-cells in each of the groups is evaluated from the proportion pale/dark B-cells. In control animals this is about 50/50, in both experimental groups there is a marked predominance of pale B-cells. During normal pregnancy, a shift occurs towards a majority of pale B-cells. In the offspring of diabetic mothers, the ratio does not further change during gestation. It can be concluded that the disturbance in B-cell stimulation and the development of gestational diabetes in offspring of diabetic mothers is associated with a maximal recruitment of the B-cells already in basal non-pregnant condition.
    Diabetes Research and Clinical Practice 08/1998; 41(1):9-14. · 2.54 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: We studied the long-term effects of maternal diabetes mellitus on the offspring of experimentally induced diabetic Wistar rats. When stressed by an intravenous glucose load, the adult female offspring had impaired glucose tolerance and developed gestational diabetes mellitus when pregnant. Our results show that even mild diabetes mellitus induces an abnormal intrauterine milieu that causes morphological and functional changes in fetal development with consequences for later life.
    Diabetes 01/1992; 40 Suppl 2:106-8. · 8.47 Impact Factor