Abstract
Rats starved for 30 h were injected with trace amounts of [3-14C]acetoacetate and .beta.-hydroxy[3-14C]butyrate 1 h after ischemic limb injury in a 20.degree. C environment, and the concentrations and radioactivities of blood ketone bodies were determined at intervals. Starvation alone raised the rates of production and utilization of .beta.-hydroxybutyrate plus acetoacetate about 3.7-fold, but lowered their metabolic clearance rates by about 50%. In the starved rat ketone-body oxidation could account for up to 30% of whole body O2 consumption. Injury in starved rats lowered the rates of production and utilization of .beta.-hydroxybutyrate and acetoacetate, the combined fall of about 37% slightly exceeding the concomitant fall in whole-body O2 consumption. The concentration of .beta.-hydroxybutyrate decreased after injury, but its metabolic clearance rate was unaltered; the concentration of acetoacetate rose slightly and its metabolic clearance rate fell.

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