Hypophyseo-Adrenal Function in Diabetic Angiopathy

Abstract

It has been demonstrated that alterations in the corticotrophin-glucocorticoid system follow the extreme changes in carbohydrate metabolism which occur in diabetic patients. In acidosis and hypoglycaemia there is a transitory pathological increase in the plasma cortisol level and in the urinary 17-OHCS excretion. If the diabetes is satisfactorily controlled – even in labile patients – the average values are normal. In satisfactorily controlled angiopathic patients a pathologically increased hormone production cannot be demonstrated. In the uraemic phase of the Kimmelstiel-Wilson syndrome the function of the adrenal cortex deteriorates.

Hypophyseo‐adrenocortical Function in Diabetes Mellitus

“…second possibility is that the photometric method used for the determination of plasma 17-0HCS (15) may give false elevated values in diabetics (6,20,24). This is not the case with the fluorimetric method used in the present study (19).…”

“…However, determinations of corticosteroids in plasma or of corticoid metabolites in the urine have given conflicting information about the function of the adrenal cortex in diabetics. Normal baseline values of urinary 17-hydroxycorticosteroids (l7-0HCS) (12,16,18,21,24), urinary 17-ketogenic steroids (l7-KGS) (12) and normal baseline values of plasma 17-0HCS (12,21,24) have been found in diabetics with and without angiopathy. In the above investigations the patients were selected regardless of whether they received insulin or not; blood sugar level was fairly well regulated, Serio et al (23) found normal circadian rhythms and normal baseline values of f1uorimetrically determined plasma cortisol in eight non-insulin-treated diabetics with satisfactory blood sugar regulation.…”

“…Hyperglycaemia with ketoacidosis, during which the adrenocortical activity is increased (12,14,24,25), occurs relatively rarely in insulin-treated diabetics. On the other hand, considerable fluctuations in the blood sugar undoubtedly occur dai1ĩ n many insulin-treated juvenile diabetics, which might well be the cause of an increased pituita~ adrenocortical activity in such patients.…”