“Steroid Diabetes” and Alkalosis Associated With Cushing's Syndrome: Report of Case, Isolation of 17-Hydroxy-Corticosterone (Compound F) From Urine, and Metabolic Studies*

THE diabetes mellitus which sometimes occurs in association with hyperfunctioning lesions of the adrenal cortices is most reasonably explained on the basis of excessive production of adrenal cortical hormones which have carbohydrate activity, that is, the 11-oxygenated and 11, 17-oxygenated steroids. Of these, the most potent are 17-hydroxy-ll-dehydrocorticosterone (compound E) and 17-hydroxycorticosterone (compound F), the latter having slightly stronger carbohydrate effects than the former.1 If the foregoing reasoning is correct, such diabetes, when severe, should have the same general characteristics as the “steroid diabetes” produced by Ingle and his associates (6, 7) in rats by the administration of compound E or compound F, and these characteristics should serve to distinguish it from the usual type of diabetes which is commonly observed in children and young adults: i) It should be relatively insensitive to insulin, Ingle and his associates (7) having failed to control glycosuria completely in some of their rats with as much as 1,000 units of insulin daily; ii) it should become mild when food is withheld, so that glycosuria diminishes markedly or disappears, and iii) since one of the effects of the carbohydrate-active adrenal hormones is to stimulate protein catabolism, it should regularly be associated with a negative nitrogen balance, even when glycosuria is minimal or absent.