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Hormonal enteroinsular axis in newborn infants of insulin-treated diabetic mothers
1Department of Pediatrics, University of Oulu, Finland.
Insights
Infants of diabetic mothers (IDM) show higher cord blood glucose and C-peptide. Human milk feeding rapidly corrects hypoglycemia in IDM, indicating postnatal maturation of the enteroinsular axis in both IDM and control infants.
Area of Science:
- Endocrinology
- Neonatal Physiology
- Metabolic Disorders
Background:
- Diabetic pregnancies can lead to increased amniotic fluid glucose.
- This may influence the hormonal enteroinsular axis maturation in newborns.
- Understanding this axis is crucial for managing neonatal outcomes.
Purpose of the Study:
- To investigate if elevated amniotic glucose in diabetic pregnancies accelerates enteroinsular axis maturation.
- To compare hormonal profiles and glucose regulation in infants of diabetic mothers (IDM) versus controls.
Main Methods:
- Measured cord blood glucose, C-peptide, glucagon, enteroglucagon, and GIP in IDM and control infants.
- Assessed these parameters before and after the first human milk feed in both groups.
- Utilized nasogastric tube feeding for standardized milk intake.
Main Results:
- IDM had higher cord blood glucose and C-peptide; levels fell postnatally.
- Enteroglucagon and GIP increased post-feed in both groups.
- Human milk feeding corrected hypoglycemia in IDM within 2 hours without worsening hyperinsulinemia.
Conclusions:
- Enteral feeding with human milk is effective in managing early postnatal hypoglycemia in IDM.
- The enteroinsular axis appears to mature postnatally in both IDM and control infants.
- No significant differences in postprandial hormone concentrations suggest similar maturation rates after the first feed.
Abstract:
To study whether the increased glucose levels in the amniotic fluid during diabetic pregnancies induce an early maturation of the hormonal enteroinsular axis, we measured blood glucose levels and plasma concentrations of C-peptide, pancreatic glucagon, enteroglucagon, and gastric inhibitory polypeptide (GIP) in cord blood from 18 newborn infants of insulin-treated diabetic mothers (IDM) and 18 infants of nondiabetic mothers. In addition, we studied the same parameters in 20 IDM and 12 control infants before and after their first feed comprising human milk (5 mL/kg), given by nasogastric tube at the age of 2 h. The IDM had significantly higher blood glucose levels and plasma C-peptide concentrations in their cord blood than the control infants, which was followed postnatally by a substantial fall in these levels, whereas a more modest decrease could be seen in the control infants. Circulating enteroglucagon and GIP concentrations at the age of 2 h were significantly higher than those observed in cord blood in both the IDM and the control infants, but the IDM had significantly lower blood glucose levels, higher plasma C-peptide, and lower enteroglucagon concentrations before the first feed. There was a significant increase in blood glucose levels after the feed in both the IDM and the control infants, and the concentrations 2 h after feeding were of the same magnitude in the two groups. No significant C-peptide response could be observed in either group, but the IDM continuously had higher C-peptide concentrations. A significant enteroglucagon and GIP response could be seen in the IDM, whereas the controls exhibited only a GIP response. However, no significant differences were found between the two groups in the absolute postprandial plasma concentrations of these hormones. Our results show rapid, substantial postnatal changes in circulating concentrations of enteroinsular hormones in both IDM and control infants. Enteral feeding with human milk corrects early postnatal hypoglycemia within 2 h in most IDM without causing any exacerbation of their hyperinsulinemia. The absence of any C-peptide response to the first feed and of any observed differences between IDM and normal infants in absolute concentrations of enteroglucagon and GIP after the first feed suggests that the enteroinsular axis matures postnatally in both groups of infants.