Related Experiment Videos
Cardiac septal hypertrophy in hyperinsulinemic infants
Insights
Infants of diabetic mothers (IDM) with septal hypertrophy showed profound hypoglycemia. Fetal hyperinsulinemia, not hyperglycemia, may directly cause this cardiac hypertrophy in IDM.
Area of Science:
- Neonatalogy
- Pediatric Cardiology
- Endocrinology
Background:
- Infants of diabetic mothers (IDM) are at risk for cardiac abnormalities.
- Septal hypertrophy is a recognized complication in some IDM.
- The exact cause of septal hypertrophy in IDM remains unclear.
Purpose of the Study:
- To investigate the relationship between septal hypertrophy and neonatal clinical findings in infants of diabetic mothers.
- To explore the potential role of fetal hyperinsulinemia in the development of septal hypertrophy.
Main Methods:
- Echocardiography was used to determine septal hypertrophy (>= 6 mm) in infants.
- Clinical data including hypoglycemia, hypocalcemia, polycythemia, and birth asphyxia were collected.
- Infants with and without septal hypertrophy were compared.
Main Results:
- Five of 18 infants of diabetic mothers and one infant with nesidioblastosis exhibited septal hypertrophy.
- No correlation was found between septal hypertrophy and hypocalcemia, polycythemia, or birth asphyxia.
- All infants with septal hypertrophy presented with profound neonatal hypoglycemia, unlike those without.
Conclusions:
- Profound neonatal hypoglycemia in infants with septal hypertrophy is consistent with fetal hyperinsulinemia.
- The study hypothesizes that fetal hyperinsulinemia, rather than fetal hyperglycemia, directly contributes to septal hypertrophy in infants of diabetic mothers.
Abstract:
One infant with nesidioblastosis, and five of 18 infants of diabetic mothers had echocardiographically determined septal hypertrophy (greater than or equal to 6 mm). No correlation was found between the septal hypertrophy and the presence of hypocalcemia, polycythemia, birth asphyxia, or other observed clinical findings. All of the infants with septal hypertrophy, however, had profound hypoglycemia shortly after birth in contrast to those infants without septal hypertrophy. Macrosomic IDM have intrauterine hyperglycemia and hyperinsulinemia. The presence of profound neonatal hypoglycemia is consistent with the metabolic effects of significant neonatal hyperinsulinemia which is also present in the fetus. Infants with nesidioblastosis also have fetal hyperinsulinemia. Recent investigations have suggested an important role for insulin in the developing heart since it is rich in insulin receptors and contains marked insulin degrading capacity. Although fetal hyperglycemia has been suggested as the cause of septal hypertrophy in IDM, we hypothesize that fetal hyperinsulinemia contributes directly to the spinal hypertrophy.