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Glucoregulatory disorders in school refusal students

N Iwatani¹, T Miike, Y Kai

¹Department of Child Development, Kumamoto University School of Medicine, Japan.

Clinical Endocrinology

|November 28, 1997

Summary

School refusal students exhibit impaired glucose metabolism, with higher blood glucose levels and suppressed insulin response during oral glucose tolerance tests. Emotional distress likely contributes to these glucoregulatory disorders.

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Area of Science:

Endocrinology
Neuroscience
Psychiatry

Background:

Previous studies linked school refusal to autonomic nervous system disorders and cerebral hypoperfusion.
Severe stress is known to impact glucoregulatory metabolism.
Emotional distress in students may manifest in physiological dysregulation.

Purpose of the Study:

To investigate glucose metabolism in school refusal students using the oral glucose tolerance test (OGTT).
To assess blood glucose, insulin, glucagon, and growth hormone levels in relation to emotional distress.

Main Methods:

A three-hour oral glucose tolerance test (OGTT) was administered to 81 school refusal students (ages 11-19).
Blood samples were collected at intervals to measure blood glucose (BG), immunoreactive insulin (IRI), pancreatic glucagon (IRG), and growth hormone (GH).

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Self-rating depressive scale (SDS) was used to assess emotional difficulties.

Main Results:

School refusal students showed significantly higher BG levels and cumulative BG (sigma BG) compared to normal controls.
A relative suppression of insulin secretion was observed, indicated by a lower insulin/glucose ratio (sigma IRI/sigma BG).
A paradoxical increase in growth hormone (GH) was noted in some students post-glucose ingestion.

Conclusions:

Glucoregulatory disorders, including hyperglycemia, are prevalent in school refusal students and may stem from emotional distress.
Autonomic nervous system dysfunction, hypothalamic neuropeptide derangement, and hormonal imbalances may contribute to these metabolic changes.
The brain's energy demands during stress might lead to increased blood glucose concentrations as a compensatory mechanism.