JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
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Zinc supplementation mitigates its dyshomeostasis in experimental diabetic rats by regulating the expression of zinc transporters and metallothionein.

Zinc depletion during diabetes projects a role for zinc nutrition in this condition. This study explored whether zinc supplementation annuls diabetes-induced zinc dyshomeostasis through modulation of zinc transporters and metallothionein. Groups of hyperglycemic rats were exposed for six weeks to supplemental zinc (5 or 10-times the normal level). Intracellular zinc concentration and zinc transporter and metallothionein expression levels in different tissues were analysed. Depleted zinc concentrations in different organs were restored by zinc supplementation. Zinc ions cross biological membranes with the aid of membrane proteins, belonging to zinc transporter families - ZIPs (responsible for the influx) and ZnTs (responsible for intracellular traffic/efflux). Up-regulated expression levels of zinc efflux proteins and influx proteins were beneficially modulated by zinc treatment, which also induced metallothionein expression in tissues to mitigate oxidative stress. Thus, zinc supplementation has a significant benefit in controlling zinc fluxes during diabetes, exerted through a protective influence on the modulation of the expression of zinc transporters and metallothionein.

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