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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. "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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