Role of zinc supplementation in type II diabetes mellitus

C. B. Niewoehner, John I. Allen, Maria Boosalis, Allen S. Levine, John E. Morley

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Zinc is required for normal immune function and taste acuity and enhances the in vitro effectiveness of insulin. Impaired immune function and taste have been reported in diabetic subjects, and decreased serum zinc levels and hyperzincuria occur in some diabetic subjects and animals. Subjects with type II diabetes were examined to determine whether the similar effects of zinc depletion and diabetes are causally related. Low serum zinc levels were found in 16 of 180 subjects (9 percent). There was no correlation between serum zinc and glycosylated hemoglobin levels. Natural killer cell activity did not differ between diabetic subjects (n = 28) and control subjects (n = 38) and did not correlate with serum zinc levels. T lymphocyte response to phytohemagglutinin was lower in diabetic subjects than in control subjects (70 ± 10 versus 103 ± 7 × 103 counts per minute) but was not lowest in those with the lowest zinc levels. Taste thresholds for hydrochloric acid, sucrose, sodium chloride, and urea were elevated in diabetic subjects (n = 28) versus control subjects (n = 10), but thresholds did not correlate with glycosylated hemoglobin or serum zinc levels. Zinc supplementation in nine diabetic subjects had no effect on the glycosylated hemoglobin level, natural killer cell activity, or taste thresholds, but it did increase mitogen activity in those with the lowest initial phytohemagglutinin responses. It is concluded that zinc deficiency occurs in a subset of subjects with type II diabetes but is not related to diabetes control and does not explain decreased taste acuity. Zinc deficiency may play a role in abnormal immune function in type II diabetes mellitus.

Original languageEnglish (US)
Pages (from-to)63-68
Number of pages6
JournalThe American Journal of Medicine
Issue number1
StatePublished - Jul 1986

Bibliographical note

Funding Information:
From the Sections of Endocrinology and Metabolism, Primary Care, and Gastroenterology, Veterans Administration Medical Center, and the Department of Medicine, University of Minnesota, Minneapolis, Minnesota. This work was supported by Veterans Administration Merit Review Funds. Requests for reprints should be addressed to Dr. C. B. Niewoehner, Endocrinology and Metabolism Section (111G), Veterans Administration Medical Center, 54th Street and 48th Avenue South, Minneapolis, Minnesota 55417. Manuscript accepted May 2, 1985.


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