HYPERZINCURIA IN INSULIN TREATED DIABETES-MELLITUS - ITS RELATION TO GLUCOSE-HOMEOSTASIS AND INSULIN ADMINISTRATION

To elucidate some pathogenic factors of diabetic hyperzincuria 60 adult insulin treated diabetic out-patients (40 males and 20 females) were studied, all with normal serum creatinine concentrations and absence of proteinuria during a 24-h period. Diabetic males and females both had significantly (P < 0.01) increased Zn excretion rates (1.14 .+-. 0.06 (SEM [standard error of the mean]) .mu.mol/mmol creatinine and 1.37 .+-. 0.10 .mu.mol/mmol creatinine) compared with normal males and females (0.55 .+-. 0.06 and 0.48 .+-. 0.08, respectively). The urinary Zn excretion rate correlated positively with the degree of glycosuria (r = 0.36, P < 0.01), but was not associated with the duration of the disease. Serum Zn levels gave no evidence of a state of Zn depletion in these patients. Zn originating from a diabetic bone loss and exogenous insulin administration accounted for only a small part of the hyperzincuria. Compensatory hyperabsorption and/or increased Zn content in the diabetic diet may explain the lack of Zn depletion in the presence of hyperzincuria.