Abstract
Conclusions
These data suggest that the increased Qo2 of hy-perthyroid brain is especially associated with carbohydrate oxidations. The results with inhibitors further indicate that this greater respiration depends on proportional increases of both dehydrases and oxidases in the normal cell but stronger concentrations of narcotics must be used to clinch this point. These results do not exclude Haffner's,3 or allied hypotheses, which regard an increased glycolysis as the essential metabolic effect of hyperthyroidism and the increased Qo2 as a secondary consequence.
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