Competition between sodium reabsorption and gluconeogenesis in kidneys of steroid-treated rats.

Kidneys of rats treated with methylprednisolone show altered substrate requirements for sodium reabsorption when perfused in vitro. Such kidneys synthesize glucose from lactate at twice the rate of control. Optimum sodium reabsorption is not seen with glucose, which is normally the preferred substrate. Sodium reabsorption is restored toward normal by the combination of glucose and butyrate, by pyruvate, or by 3-mercaptopicolinate. All of these results point to a metabolic adaptation in the kidney; butyrate may improve sodium reabsorption by sparing glucose, pyruvate is a gluconeogenic precursor and an effective fuel of respiration, and 3-mercaptopicolinate is an inhibitor of gluconeogenesis. In kidneys from rats treated with methylprednisolone there is an increased requirement for metabolic energy because of the increased rate of gluconeogenesis. It is suggested that the availability of energy from glucose oxidation is limited in part by the diversion of pyruvate back to glucose. Under these special circumstances, gluconeogenesis competes with sodium reabsorption in the intact kidney.