Abstract
Insulin hypoglycemia elicited a prompt increase in 17-hydroxycorticosteroid (17-OHCS) secretion in the dog. It is of limited duration in spite of continued hypoglycemia. When insulin hypoglycemia was prevented by simultaneously administered 50% glucose, no increase in 17-OHCS secretion followed. The administration of insulin during a dexamethasone suppression test failed to give a significant 17-OHCS response. Neither pituitary nor adrenal unrespon-siveness is a factor in limiting this 17-OHCS secretory response.