Author(s): BrandoNeto J, da Silva CA, Figueiredo NB, Shuhama T, da Cunha NF, , BrandoNeto J, da Silva CA, Figueiredo NB, Shuhama T, da Cunha NF,
Abstract Share this page
Abstract Acute or chronic zinc administration may cause hyperglycemia in experimental animals. These findings are attributed to permissive actions of glucocorticoids and glucagon upon hepatic gluconeogenesis and glycogenolysis. The effect of Zn(+)+ on plasma glucose, C-peptide, glucagon, and cortisol was investigated in healthy and insulin-dependent diabetes mellitus (IDDM) patients. Ten normal individuals (5 of each sex, aged 24.10 +/- 1.96) and 10 IDDM (5 of each sex, aged 25.20 +/- 8.10) were tested at 7:00 AM after 12-h fast. Twenty-five mg of Zn(+)+ were administered intravenously during 1 min, and blood samples were collected from the contralateral arm at 0, 3, 30, 60, 90 and 120 min after Zn(+)+ injection. The plasma levels of glucose, C-peptide, and glucagon remained constant throughout the experimental period in both groups studied. Plasma cortisol levels decreased significantly, which is consistent with our previous findings. These results suggest that, in contrast to experimental animals, acute Zn(+)+ administration, despite decreasing cortisol levels, does not change carbohydrate metabolism in human beings.
This article was published in Biometals
and referenced in Journal of Drug Metabolism & Toxicology