To study the effects on the fetus of variations in maternal glucose tolerance, a 25 g rapid intravenous glucose tolerance test was performed at or about 32 weeks gestation in 917 randomly selected nondiabetic women with singleton pregnancies. The results were withheld from the patients and their obstetricians and paediatricians, and no treatment or advice was offered. Fasting plasma glucose and indices of glucose disposal (including a new index which we have termed "summed glucose") were distributed unimodally, with no evidence of a separate pathological group towards the diabetic end of the distributions. Significant associations were found between maternal glucose metabolism and various measures of neonatal nutrition and morbidity, including the incidence of congenital malformations and morbidity related to asphyxia, suggesting that variations within the normal range in maternal glucose metabolism can influence growth and development in the fetus. These relationships were continuous throughout the range of maternal glucose tolerance and were not of predictive value in individual cases.

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To study insulin response and insulin sensitivity a glucose infusion test was devised. Twenty normal non-pregnant and twenty normal pregnant women had an intravenous glucose tolerance test followed by a glucose infusion test. In a normal pregnant group at 38-40 weeks gestation (n = 20) the plasma insulin response was found to be 3.7 times greater than that observed in a normal non-pregnant group (n = 20), while in the normal pregnant group the insulin sensitivity index was only 18 per cent of that observed in the non-pregnant group. Intravenous glucose tolerance in the non-pregnant women was observed to correlate with the insulin sensitivity index (r = 0.61, p less than 0.05) but in the pregnant women it correlated with the insulin response (r = 0.66, p less than 0.01). These findings support the hypothesis that in the non-pregnant state intravenous glucose tolerance may be primarily related to insulin sensitivity while during pregnancy it may be related to the degree of compensatory hyperinsulinism.

One hundred twelve women with impaired glucose tolerance (IGT) diagnosed by intravenous glucose tolerance test (IVGTT) after pregnancy were followed up for a period of up to 22 yr (mean 12.9 yr). About one-third have been treated with chlorpropamide and the others by diet only. At the final assessment, approximately 35% had abnormal intravenous glucose tolerance and less than 7% overt diabetes. Chlorpropamide did not prove significantly more effective than diet only. Factors associated with deterioration in glucose tolerance were age at diagnosis and follow-up and the initial fasting plasma glucose (FPG) level (greater than or equal to 5.8 mM), but obesity was less important, although it was associated with an increased rate of vascular complications. Tests for islet cell antibodies (ICA) were weakly positive in 12.5% of 72 subjects and in only 0.5% of an unselected population; they did not correlate with the final state of glucose tolerance. Only three patients developed insulin-dependent diabetes (IDDM) and did so before the ICA study was started. A comparison is made between the results reported by O'Sullivan in patients diagnosed as having gestational diabetes, only 2% of whom still had abnormal oral glucose tolerance postpartum, and the results of our patients, all of whom had IGT after pregnancy. In spite of differences of technique and in the populations studied, the prevalence of IGT and overt diabetes at follow-up was significantly less in the Aberdeen series, who were initially a higher risk group. It seems probable that this is mainly attributable to dietary treatment in the follow-up period as O'Sullivan's cases were treated only during pregnancy.

A method to assess the average percentage of fetal fat with respect to other fetal tissue is described. This method was then used to assess the percentage of fat in 13 normal fetuses who had a magnetic resonance imaging (MRI) examination late in pregnancy (38-41 weeks). The scans of a further 13 fetuses of diabetic mothers and one case of intrauterine growth retardation (IUGR), all of whom had MRI examinations in the last 3 years, were reviewed and similar calculations were carried out. Whilst the percentage fat range in the normal group was large, it was still possible to discern a difference between the normal, diabetic and IUGR cases.