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Glucose metabolism and insulin secretion in infants with symptomatic ventricular septal defect
K H Lundell1, K G Sabel, B O Eriksson
1Department of Paediatrics, Central Hospital of Jönköping, Gothenburg, Sweden.
Insights
Infants with symptomatic ventricular septal defect (VSD) show normal glucose tolerance but have altered insulin responses. Despite higher insulin secretion, circulating insulin levels are lower, suggesting increased insulin binding or liver extraction.
Area of Science:
- Pediatrics
- Endocrinology
- Cardiology
Background:
- Symptomatic infants with ventricular septal defect (VSD) often exhibit growth retardation.
- Metabolic alterations, particularly glucose and insulin metabolism, may be associated with VSD.
Purpose of the Study:
- To investigate glucose tolerance and insulin secretion in infants with symptomatic VSD.
- To compare metabolic profiles between VSD infants and healthy controls.
Main Methods:
- Intravenous glucose tolerance test (IVGTT) performed on 19 infants with symptomatic VSD and 14 healthy infants.
- Plasma glucose, insulin, and C-peptide levels were measured.
- Insulin secretion rate calculated from C-peptide levels.
Main Results:
- VSD infants were growth retarded but demonstrated normal glucose tolerance, including fasting glucose and glucose disappearance rate.
- Insulin levels in plasma were significantly lower in VSD infants post-glucose load.
- Calculated insulin secretion rate was significantly elevated in VSD infants compared to controls.
Conclusions:
- Infants with symptomatic VSD maintain normal glucose tolerance despite growth deficits.
- VSD is associated with an increased insulin secretion rate but decreased circulating insulin levels.
- This discrepancy suggests enhanced insulin binding to peripheral receptors or increased hepatic insulin extraction in VSD infants.
Abstract:
Nineteen infants with symptomatic ventricular septal defect (VSD) were examined on, altogether, 26 occasions, when each was given an intravenous glucose tolerance test (IVGTT); concentrations of insulin- and C-peptide in plasma were determined. Comparisons were made with 14 healthy infants of the same age. The VSD infants were growth retarded with lower weight/age and length/age ratios. Glucose tolerance as indicated by glucose fasting levels and response to intravenous glucose tolerance test, including glucose disappearance rate, did not differ between the two groups. In response to the glucose load, insulin in plasma was significantly less in VSD infants. In response to the IVGTT, insulin secretion rate calculated from C-peptide levels in plasma was significantly elevated in the VSD group. We conclude that compared to healthy infants, those with symptomatic VSD have normal glucose tolerance, increased secretion rate of insulin, but decreased levels of circulating insulin in response to an intravenous glucose load. We suggest this is so because binding of insulin to peripheral receptors and/or insulin extraction in the liver somehow increases.
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