Glucose tolerance and insulin secretion in children of mothers with pregestational IDDM or gestational diabetes

Abstract

Since Pedersen's fundamental work [1] the metabolic situation in infants of mothers with diabetes mellitus during pregnancy has been investigated in a number of studies [2][3][4]. While most authors focussed on altered glucose homeostasis during neonatal life, it remains unclear if these alterations do persist or resolve in later life. Clinical investigations during childhood indicated elevated frequencies of impaired glucose tolerance (IGT) in the offspring of mothers with diabetes during pregnancy [5,6]. Some authors reported alterations of insulin secretion such as hyperinsulinaemia [6,7] which is known to play a key role in the development of metabolic and cardiovascular disturbances in adulthood [8]. Experimental studies in rats displayed long-term alterations of glucose tolerance and insulin secretion due to the induction of maternal gestational hyperglycaemia which leads to fetal and neonatal hyperinsulinism [9][10][11][12][13].However, only a very small number of studies are available which compared glucose metabolism and Diabetologia (1997Diabetologia ( ) 40: 1094Diabetologia ( -1100 Glucose tolerance and insulin secretion in children of mothers with pregestational IDDM or gestational diabetes Summary The offspring of mothers with diabetes mellitus during pregnancy are presumed to develop altered glucose homeostasis. We analysed metabolic parameters at birth and glucose tolerance and insulin secretion during oral glucose tolerance tests at 1-9 years of age in 129 children born to mothers with pregestational insulin-dependent diabetes (IDDM) and 69 infants of gestational diabetic mothers. Newborns of IDDM mothers displayed higher insulin (p < 0.001), glucose (p < 0.05), and insulin/glucose ratios (p < 0.002) than newborns of gestational diabetic mothers. During childhood, frequencies of impaired glucose tolerance (IGT) rose in infants of IDDM mothers from 9.4 % at 1-4 years to 17.4 % at 5-9 years of age, while in children of gestational diabetic mothers an increase from 11.1 % up to 20.0 % was observed. Offspring of gestational diabetic mothers displayed higher stimulated blood glucose (p < 0.025) than infants of IDDM mothers, while children of IDDM mothers showed higher stimulated insulin (p < 0.025), accompanied by increased fasting and stimulated insulin/glucose ratios (p < 0.05 and p < 0.02, respectively). Stimulated insulin in childhood was positively correlated to insulin at birth (p < 0.05). Furthermore, insulin/glucose ratio in childhood showed a positive correlation to insulin (p < 0.01) and insulin/glucose ratio at birth (p < 0.005). In conclusion, a pathogenetic role of fetal and neonatal hyperinsulinism for the development of IGT in both groups of infants of diabetic mothers is suggested, in particular for early induction of insulin resistance in the offspring of mothers with pregestational IDDM. [Diabetologia (1997)

Relation between fetal anthropometric parameters and cord blood adiponectin and high-sensitivity C-reactive protein in gestational diabetes mellitus

“…Women who had no values meeting a NDDG criteria were included in the NGT group. Those who had only one value exceeding the threshold of the criteria were excluded from the study (22).…”

Fetal growth and developmental programming

“…Furthermore, impaired glucose tolerance and obesity in adults due to a diabetic intra-uterine environment is independent of the genetic background [10,11,39] .…”

Significant effects of mild endogenous hormonal changes in humans: considerations for low-dose testing.

“…For example, during pregnancy, the screening for gestational diabetes uses both different test and cutoff values of blood glucose (Table 1) (68) because during pregnancy the outcome of the fetus also must be taken into account. Gestational diabetes is associated with significant maternal and fetal morbidity and longterm consequences for the offspring (increased weight, glucose intolerance, or even poorer intellectual performance, and psychomotor development) (69)(70)(71). Fetal and neonatal hyperinsulinemia in offspring of diabetic mothers causes immediate neonatal hypoglycemia and subsequent development of childhood obesity and glucose intolerance (69).…”