Renal reabsorption and utilization of hydroxybutyrate and acetoacetate in starved rats.

Are there increases in the renal reabsorption (R) and utilization (Q) of ketoacids during starvation? R and Q of D-3-hydroxybutyrate and acetoacetate were measured in anesthetized normally fed (C) and 3-day starved (S) rats, using clearance and arteriovenous extraction methods. R was nearly complete in both groups at low filtered ketoacids loads (less than 2mumol/g X min). At higher filtered loads, R of the two ketoacids increased in proportion to their filtered loads (r2 greater than 0.95) but with significantly steeper slopes in the S than in the C group; fractional R of the two ketoacids were significantly higher in the S than in the C animals. Saturable and nonsaturable components for ketoacid reabsorption were evident, but only the nonsaturable component was significantly increased with starvation. Increased R of ketoacids during starvation was in the absence of changes in the initial rates of hydroxybutyrate influx into isolated rat renal brush-border membrane vesicles. Thus the rate-limiting step for ketoacid reabsorption through the nonsaturable pathway may not be located at the luminal membrane of the proximal cells. The increases in R of ketoacids in the S group were associated with simultaneous decreases in the net rates of renal utilization of the two ketoacids. Thus increased renal conservation of ketoacids is a transport and not a metabolic event. Overall, during complete starvation, both the increased R and the decreased renal Q of the ketoacids contribute to increase the availability of these metabolites to other organs.