The effect of cortisone on the intermediary metabolism of epiphyseal cartilage from rats

Total glucose stores per cell are reduced by half in tibial epiphyseal cartilage from rats after 3 days of cortisone treatment, and the ability to produce lactate in vitro without added substrate is abolished. Cortisone reduces lactate production from exogenous glucose to 30% of normal. The pentose shunt pathway and lactate formation from pyruvate also are decreased. In contrast, 14CO 2 evolution from glucose-6- 14C or labeled pyruvate is unaffected by cortisone treatment suggesting that the potential rate of pyruvate oxidation via the citric acid cycle is relatively insensitive to the hormone. High levels of pyruvate in vitro inhibit lactate formation from labeled glucose by over 90% in normal and cortisone-treated tissue while doubling 14CO 2 evolution from glucose-1- 14C. Total lactate production is depressed while glucose utilization is stimulated suggesting that pyruvate can inhibit glycolysis in cartilage tissue and divert glucose to alternate fates such as the pentose shunt and glycogen synthesis. The controlling influence of such hormonal and metabolic mechanisms on glycolysis may contribute significantly to the marked atrophic effect of glucocorticoids on growth cartilage as well as to the phenomenon of decreased peripheral glucose utilization induced by these hormones.