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- W2110105087 endingPage "169" @default.
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- W2110105087 abstract "Genetic studies suggest that Zn transporters such as ZnT8 play a role in insulin secretion by pancreatic β-cells; however, little is known about the dynamic roles of Zn trafficking pathways on β-cell physiology. To test the acute effects of the inflammatory cytokines interleukin 1β (IL1β) and tumor necrosis factor α (TNFα) on Zn homeostasis, the mRNA expression profile of Zn transporters of the ZnT and ZIP families was examined. Exposure of MIN6 cells or primary murine islets to IL1β or TNFα altered the mRNA expression profile of Zn transporters; most notable was decreased ZnT8 mRNA levels. siRNA-mediated gene knockdown was used to examine the effects of decreased ZnT8 expression in primary dispersed murine islet cells from C57/BL6 mice and MIN6 cells. ZnT8 knockdown in these murine islets led to reduced glucose stimulated insulin secretion without altering the total cellular insulin content or cell viability at normal or supraphysiological Zn concentrations. The labile Zn content determined by flow cytometry after loading with the Zn-specific sensor FluoZin-3 AM was decreased in MIN6 cells following ZnT8 knockdown or IL1β treatment. These results suggest that an acute decrease in ZnT8 levels impairs β-cell function and Zn homeostasis, and may contribute to inflammatory cytokine-induced alterations in β-cell function." @default.
- W2110105087 created "2016-06-24" @default.
- W2110105087 creator A5010015600 @default.
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- W2110105087 creator A5087803746 @default.
- W2110105087 date "2010-05-27" @default.
- W2110105087 modified "2023-09-26" @default.
- W2110105087 title "Acute cytokine-mediated downregulation of the zinc transporter ZnT8 alters pancreatic β-cell function" @default.
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- W2110105087 doi "https://doi.org/10.1677/joe-09-0420" @default.
- W2110105087 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3088990" @default.
- W2110105087 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20508080" @default.
- W2110105087 hasPublicationYear "2010" @default.
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