Summary1) 50 mg of ACTH injected to normal and diabetic subjects induce an adrenal cortex reaction, which is characterized by a drop in the eosinophil count and a rise in the urinary 17 ketosteroids. The intensity of the response is the same in both groups of subjects.ACTH provokes in normal subjects a small increase in the blood sugar level; on the contrary, in diabetics treated or untreated by insulin, the rise of glycemia and of glycosuria after injection of ACTH is important; this last action is not due to an exaggerated reaction of the adrenal cortex of these patients.2) Injections of ACTH decrease in normal and diabetic subjects the sensitivity to insulin; this action of ACTH is more important in diabetics than in normal subjects.3) Hypoglycemia due to insulin stimulates the adrenal cortex of normal and diabetic subjects. In diabetics, a decrease in the glycemia does not stimulate the adrenal cortex as long as the blood sugar level remains above 0,70 gr. 0/00.4) Transient or prolonged hyperglycemia has no action on adrenal cortex activity of normal and diabetic subjects.5) In diabetics treated by insulin, the suppression of this treatment has no action on the activity of the adrenal cortex if it is only followed by hyperglycemia; if acidosis and acetonuria occur, the adrenal cortex stimulation is characterized by a drop in the eosinophil count, if the acetonuria is small, bv a drop in the eosinophil count and a rise in the urinary 17 ketosteroids if acetonuria is marked; as stimulation of the adrenal cortex causes an increase of acetonuria, the suppression of insulin in such patients induces a vicious circle which leads them into diabetic coma.6) In severe diabetics, acute infections, traumatisms, cerebral accident and acute cardiac failure stimulate the adrenal cortex; this is shown by a drop in the eosinophil count, a rise in the 17 ketosteroids and, at the same time, an increase of blood sugar and acidosis. Some days later, there occurs a depression of adrenal cortex activity (rise of the eosinophil count, decrease of 17 ketosteroids) and at the same time, hypoglycemia.7) During diabetic coma, adrenal cortex activity is stimulated; this increased activity is followed by a period of adrenal cortex hypeactivity; during this period, the sensitivity to insulin is increased.These facts explain why it is often difficult to determine the insulin dose, to be administred to diabetic subjects during acidosis, infections and traumatisms and why these patients easily pass from hyperglycemia to hypoglycemia.In diabetic subjects, it is useful during critical circumstances, such as acidosis, infections, traumatisms, to study at the same time the variations in the blood sugar and in the adrenal activity; it is possible, by this procedure, to determine the periods during which it is necessary to increase or to decrease the insulin dose.