OBJECTIVES 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 w
ith school attendance. Because severe stress is known to affect glucor
egulatory metabolism, this study used the oral glucose tolerance test
(OGTT) to measure glucose metabolism in school refusal students. DESIG
N A three-hour OGTT was performed. In preparation for the test, studen
ts fasted overnight. After a fasting blood sample was drawn, students
were given solutions containing a predetermined amount of glucose base
d on their body weight (1.75 g/kg to a maximum 75 g). After glucose in
gestion, blood samples were drawn at 30, 60, 90, 120, 150, and 180 min
to measure blood glucose (BG), immunoreactive insulin (IRI), pancreat
ic glucagon (IRG) and growth hormone (GH) levels. BG levels, IRI respo
nse, cumulative BG (Sigma BG), cumulative IRI (Sigma IRI), insulin/glu
cose ratio (Delta IRI/Delta BG), and insulinogenic index (Sigma IRI/Si
gma BG) were then compared to previously reported normal control data.
As an index of emotional difficulties, the self-rating depressive sca
le (SDS) was carried out. PATIENTS Eighty-one school refusal students
(40 males and 41 females), 11-19 years of age (14.8 +/- 2.1), were stu
died. Their school refusal periods ranged from one month to eight year
s. All students were within -15 to + 20% (-0.04 +/- 8.6) of ideal body
weight. MEASUREMENTS BG levels were determined using a glucose oxidas
e reaction method. Serum hormones were measured by radioimmunoassay. R
ESULTS BG levels at all OGTT time intervals and Sigma BG were signific
antly higher in school refusal students than the normal control data (
Sigma BG: 39.5 +/- 4.4 vs 33.3 +/- 3.4 mmol/l, P < 0.01). Although the
insulin response was abnormally low relative to the prevailing hyperg
lycaemia (Sigma IRI/Sigma BG: subjects vs control = 232 +/- 129 vs 375
+/- 271, P < 0.01), normal beta cell secretory ability was speculated
(Sigma IRI: subjects vs controls = 2805 +/- 1274 vs 2523 +/- 1219 pmo
l/l). This suggests a relative suppression of insulin secretion. A par
adoxical increase of GH was observed in 19 students after glucose inge
stion. CONCLUSIONS Glucoregulatory disorders observed in school refusa
l students may be caused by emotional distress. Multiple factors inclu
ding autonomic nervous system disorders, derangement of neuropeptides
in the hypothalamus, and hormonal imbalances may also affect glucoregu
latory metabolism, predisposing these students to hyperglycaemia. We s
peculate that the glucoregulatory system compensates for decreased blo
od flow to the brain by increasing blood glucose concentrations, there
by providing sufficient glucose as the primary energy source used duri
ng normal brain metabolism.