Results of a study in healthy men suggest a causative role for hypoxia in acutely increasing glucose intolerance.
Elevated release of epinephrine is one factor mediating this effect.
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"Our results suggest that the presence
of hypoxic diseases should be evaluated
as a possible pathogenic factor in patients
suffering from metabolic disorders such
as type 2 diabetes and metabolic syndrome,"
German investigators write in the June
1st American Journal of Respiratory
and Critical Care Medicine.
Several studies have shown a close tie
between hypoxia and the emergence of
glucose intolerance, Dr. Kerstin M.
Oltmanns and colleagues from the University
of Luebeck in Germany explain in the
paper, but "experimental evidence
of a causative role for hypoxia in this
metabolic dysfunction is surprisingly
lacking."
In a double-blind, within-subject crossover
study, they tested the effects of hypoxia
versus normoxia on glucose tolerance
by decreasing oxygen saturation to 75%
under conditions of a euglycemic clamp
and monitoring the rate of dextrose
infusion needed to maintain stable blood
glucose levels.
They observed a significant decrease
in glucose infusion rate (p < 0.01)
over a period of 150 minutes after the
onset of hypoxia in conjunction with
an increase in plasma epinephrine (p
< 0.01), heart rate (p < 0.01)
and symptoms of anxiety (p < 0.05).
Of note, glucose intolerance was "closely
comparable between hypoxic and hypoglycemic
conditions (p < 0.9) despite clear
differences in stress hormonal responses,"
Dr. Oltmanns and colleagues report.
The authors caution that while "providing
evidence of a causative role for hypoxia
in acutely elevating glucose intolerance,
it remains to be carefully considered
to what extent our findings after acute
experimental short-term hypoxia can
be generalized to the typical pathologic
conditions in which frequent hypoxic
episodes are encountered over long periods."
Am J Respir Crit Care
Med 2004;169:1231-1237.
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