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Zinc ions in β-cells of obese, insulin-resistant, and type 2 diabetic rats traced by autometallography

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Søndergaard LG, Stoltenberg M, Flyvbjerg A, Brock B, Schmitz O, Danscher G, Rungby J. Zinc ions in β-cells of obese, insulin-resistant, and type 2 diabetic rats traced by autometallography. APMIS 2003;111:1147–54.

Zinc ions in the secretory granules of β-cells are known to glue insulin molecules, creating osmotically stable hexamers. When the secretory granules open to the surface, the zinc ion pressure decreases rapidly and pH levels change from acid to physiological, which results in free insulin monomers and zinc ions. The released zinc ions have been suggested to be involved in a paracrine regulation of α- and β-cells. Since zinc is intimately involved in insulin metabolism and because zinc homeostasis is known to be disturbed in type 2 diabetes, we decided to study the ultrastructural localisation of zinc ions in insulin-resistant and type 2 diabetic rats as compared to controls. By means of autometallography, the only method available for demonstrating zinc ions at ultrastructural levels, we found zinc ions in the secretory granules and adjacent to the plasma membrane. The membrane-related staining outside the plasma membrane reflects release of zinc ions during exocytosis. No apparent difference was found in the ultrastructural localisation of zinc ions when we compared the obese Zucker (fa/fa) rats, representing the insulin resistance syndrome, and the GK rats, representing type 2 diabetes, with controls. This suggests that the ultrastructural localisation of zinc ions is unaffected by the development of type 2 diabetes in rats in a steady state of glycaemia.
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Keywords: Zinc ions; autometallography; diabetes; pancreas; ultrastructure; β-cells

Document Type: Research Article

Affiliations: 1: Department of Neurobiology, Institute of Anatomy, 2: Medical Department M, 3: Institute of Pharmacology, University of Aarhus, Aarhus, Denmark 4: Medical Department C, Aarhus University Hospital, Aarhus, Denmark

Publication date: 2003-12-01

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