Elevation of serum alkaline phosphatase concentration in patients with diabetes mellitus has been observed for several years, but the source and reasons are unknown. We report our experience with 39 diabetics, 38% of whom had an unexplained elevation of serum alkaline phosphatase. Isoenzyme determinations revealed bone fraction as the predominant species. Mean fasting serum glucose was significantly higher in the group with elevated alkaline phosphatase, supporting an association between the severity of diabetes and diabetic bone disease.

The role of the glucocorticoid (type II) receptor in the Na+ retention induced by cortisol is not known. The relative contribution of mineralocorticoid (type I) and type II receptor activation to changes in urinary Na+ and K+ excretion in man was studied using spironolactone and RU486 to inhibit type I and II receptors, respectively. Normal men eating a constant daily diet received either ACTH or cortisol for 5 days. Spironolactone (400 mg/day) inhibited ACTH (80 U/day)-induced kaliuresis, but not the Na+ retention produced by ACTH or cortisol (240 mg/day) and only blunted the modest Na+ retention induced by cortisol (120 mg/day). RU486 (1200 mg/day for the first 2 day) inhibited the first day kaliuresis and carbohydrate intolerance produced by cortisol, but did not affect the Na+ retention. Thus, the kaliuresis produced by cortisol and ACTH can be attributed to type II and type I receptor activation, respectively. The failure of RU486 to inhibit the Na+ retention induced by cortisol with evidence of adequate blockade of type II receptors indicates that the Na+ retention produced by cortisol is not mediated by type II receptor activation, but is, at least in part, mediated by the type I receptor.