Abstract
Aerobic glycolysis by mouse adrenal glands is increased in vitro by ACTH, cyclic AMP and dibutyryl cyclic AMP, in a dosedependent manner. Ouabain at 10-4M increases both lactic acid and steroid output. Replacement of sodium with 60 mil potassium triples steroid production in the absence of ACTH without affecting glycolysis. Anaerobiosis stimulates glycolysis, while inhibiting steroid production, and anaerobic glycolysis is significantly depressed by ACTH. Exogenous glucose is required for the stimulation of aerobic glycolysis by ACTH, but not for the steroidogenic response. The increased lactic acid output in response to ACTH is exactly accounted for by the increased disappearance of glucose from the medium. Cyclic AMP stimulates some lactic acid formation from endogenous sources as well, but the glycolytic response is much greater in glucose-containing medium. The steroidogenic response to cyclic AMP is also independent of the presence of glucose. The effects of ACTH and cyclic AMP are additive only at suboptimal concentrations. Corticosterone, added at 0.12 mM concentration, raises the corticosterone content in the gland to the range obtained with ACTH, and it increases glycolysis as well. ACTH-and cyclic AMP-induced glycolysis may therefore be mediated to a significant extent by the raised steroid content of the gland. A second mechanism, possibly associated with lipolytic action, is not ruled out, however, as the stimulation of glycolysis by ACTH was greater, but the effect on the steroid content in the gland less, than that obtained with corticosterone, and ACTH also caused some increase in lactic acid production by the epididymal fat pad of the rat, a response requiring glucose as in the adrenal. (Endocrinology88: 845, 1971)

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