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Insulin-resistant syndromes in children
S Caprio1, S A Amiel, P Merkel
1Department of Pediatric Endocrinology, Yale University, New Haven, Conn. 06510-8064.
Insights
Puberty normally causes insulin resistance, but the body compensates. Studies in children reveal insulin resistance and increased insulin secretion are early defects in thalassaemia and Turner
Area of Science:
- Pediatric Endocrinology
- Metabolic Disorders
- Diabetes Research
Background:
- Puberty typically involves decreased insulin sensitivity, yet glucose homeostasis is maintained by increased insulin secretion.
- Understanding the precise mechanisms and implications of insulin resistance during childhood is crucial for metabolic health.
Purpose of the Study:
- To determine the site (hepatic vs. peripheral) of insulin resistance in healthy children during puberty.
- To investigate if insulin resistance extends to amino acid and free fatty acid metabolism.
- To examine the role of early insulin resistance in conditions like thalassaemia major and Turner's syndrome, which are linked to diabetes development.
Main Methods:
- Studies conducted in healthy children to assess insulin action and secretion.
- Analysis of substrate metabolism (amino acid, free fatty acid) in relation to insulin resistance.
- Comparative metabolic assessment in patients with thalassaemia major and Turner's syndrome.
Main Results:
- Identified the specific sites of insulin resistance (hepatic and peripheral) in children during puberty.
- Confirmed that insulin resistance during puberty affects not only glucose but also amino acid and free fatty acid metabolism.
- Demonstrated that insulin resistance and hyperinsulinemia are early metabolic abnormalities in thalassaemia major and Turner's syndrome, preceding diabetes onset.
Conclusions:
- Insulin resistance during puberty is a complex phenomenon affecting multiple metabolic pathways.
- Early detection of insulin resistance and hyperinsulinemia in conditions like thalassaemia major and Turner's syndrome is critical.
- These findings highlight potential therapeutic targets for preventing diabetes in at-risk pediatric populations.
Abstract:
Puberty is normally associated with a decline in tissue sensitivity to insulin. However, normal glucose homoeostasis is maintained by compensatory increases in glucose-stimulated insulin secretion. Here we describe studies performed in healthy children which have determined the site of insulin resistance (hepatic vs. peripheral) and whether this resistance extends to other substrates such as amino acid and free fatty acid metabolism. The changes in insulin action and secretion that are normally seen during puberty lead us to question the role of insulin resistance in other childhood conditions that are complicated by the later development of type I or type II diabetes, namely thalassaemia major and Turner's syndrome. These studies showed that in patients with thalassaemia and Turner's syndrome, insulin resistance and increased insulin secretion are very early metabolic defects that appear before the development of diabetes.