Hyperzincuria in insulin treated diabetes mellitus--its relation to glucose homeostasis and insulin administration.
In order to elucidate some pathogenic factors of diabetic hyperzincuria we studied 60 adult insulin treated diabetic out-patients (40 males and 20 females), all with normal serum creatinine concentrations and absence of proteinuria during a 24-h period. Diabetic males and females both had significantly (p less than 0.01) increased zinc excretion rates (1.14 +/- 0.06 (S.E.M.) mumol/mmol creatinine and 1.37 +/- 0.10 mumol/mmol creatinine) compared with normal males and females (0.55 +/- 0.06 and 0.48 +/- 0.08, respectively). The urinary zinc excretion rate correlated positively with the degree of glycosuria (r = 0.36, p less than 0.01), but was not associated with the duration of the disease. However, serum zinc levels gave no evidence of a state of zinc depletion in these patients. It was calculated that zinc originating from a diabetic bone loss and the exogenous insulin administration accounted for only a small part of the hyperzincuria. Compensatory hyperabsorption and/or increased zinc content in the diabetic diet may therefore serve to explain the lack of zinc depletion in the presence of hyperzincuria.
D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000032:analysis; D003404:Creatinine / Q000097:blood; D003920:Diabetes Mellitus / Q000652:urine*; D005260:Female; D006706:Homeostasis; D006801:Humans; D007328:Insulin / Q000008:administration & dosage / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D015032:Zinc / Q000097:blood / Q000652:urine*
D001786:Blood Glucose; D007328:Insulin; D003404:Creatinine; D015032:Zinc