Glucoregulatory disorders in school refusal students

• Noritaka Iwatani

• Teruhisa Miike

• Yumiko Kai

• Mihoko Kodama

• Hiroyo Mabe

• Akemi Tomoda

• Keiko Fukuda

• Takako Jyodoi

抄録

Our previous studies demonstrated autonomic nervous system disorders and cerebral blood hypoperfusion in school refusal students with underlying emotional distress due to fear or anxiety associated with school attendance. Because severe stress is known to affect glucoregulatory metabolism, this study used the oral glucose tolerance test (OGTT) to measure glucose metabolism in school refusal students. A three‐hour OGTT was performed. In preparation for the test, students fasted overnight. After a fasting blood sample was drawn, students were given solutions containing a predetermined amount of glucose based on their body weight (1.75 g/kg to a maximum 75 g). After glucose ingestion, blood samples were drawn at 30, 60, 90, 120, 150, and 180 min to measure blood glucose (BG), immunoreactive insulin (IRI), pancreatic glucagon (IRG) and growth hormone (GH) levels. BG levels, IRI response, cumulative BG (ΣBG), cumulative IRI (ΣIRI), insulin/glucose ratio (ΔIRI/ΔBG), and insulinogenic index (ΣIRI/ΣBG) were then compared to previously reported normal control data. As an index of emotional difficulties, the self‐rating depressive scale (SDS) was carried out. Eighty‐one school refusal students (40 males and 41 females), 11–19 years of age (14.8 ± 2.1), were studied. Their school refusal periods ranged from one month to eight years. All students were within – 15 to + 20 %(‐0.04 ± 8.6) of ideal body weight. BG levels were determined using a glucose oxidase reaction method. Serum hormones were measured by radioimmunoassay. BG levels at all OGTT time intervals and ΣBG were significantly higher in school refusal students than the normal control data (ΣBG: 39.5 ± 4.4 vs 33.3 ± 3.4 mmol/l, P  < 0.001). Although the insulin response was abnormally low relative to the prevailing hyperglycaemia (ΣIRI/ΣBG: subjects vs control = 232 ± 129 vs 375 ± 271, P  < 0.01), normal beta cell secretory ability was speculated (ΣIRI: subjects vs controls = 2805 ± 1274 vs 2523 ± 1219 pmol/l). This suggests a relative suppression of insulin secretion. A paradoxical increase of GH was observed in 19 students after glucose ingestion. Glucoregulatory disorders observed in school refusal students may be caused by emotional distress. Multiple factors including autonomic nervous system disorders, derangement of neuropeptides in the hypothalamus, and hormonal imbalances may also affect glucoregulatory metabolism, predisposing these students to hyperglycaemia. We speculate that the glucoregulatory system compensates for decreased blood flow to the brain by increasing blood glucose concentrations, thereby providing sufficient glucose as the primary energy source used during normal brain metabolism.

収録刊行物

• Clinical Endocrinology

  Clinical Endocrinology 47 (3), 273-278, 1997-09

  Wiley

キーワード

• Endocrinology, Diabetes and Metabolism
• Endocrinology

詳細情報

• CRID: 1360855569673688704
• NII論文ID: 30014621445
• DOI: 10.1046/j.1365-2265.1997.2191095.x
• ISSN: 13652265
• ISSN: 03000664
• Web Site: https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1046%2Fj.1365-2265.1997.2191095.x
• Web Site: https://onlinelibrary.wiley.com/doi/pdf/10.1046/j.1365-2265.1997.2191095.x
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