In normal nonanesthetized dogs the increased endogenous (hepatic) glucose production in insulin-induced hypoglycemia is suppressed by the infusion of D-mannose but not of D-fructose. This compensatory increase in glucose production during insulin-induced hypoglycemia is somewhat diminished but still present in dogs fasted for eight days. In fasted dogs, but not in dogs in the post-absorptive state, the infusion of DL-β-OH-butyrate is able to diminish but not to suppress this compensatory increase in glucose production. The results suggest that it is the availability of substrate to the brain rather than to the liver that sets into motion the mechanism that ultimately is responsible for the increase of glucose production, although the mechanism of the effect of β-OH-butyrate appears to be somewhat uncertain.

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