Calcineurin/NFAT signaling in the β‐cell: From diabetes to new therapeutics

@article{Heit2007CalcineurinNFATSI,
  title={Calcineurin/NFAT signaling in the $\beta$‐cell: From diabetes to new therapeutics},
  author={Jeremy J. Heit},
  journal={BioEssays},
  year={2007},
  volume={29}
}
  • J. Heit
  • Published 1 October 2007
  • Biology, Medicine
  • BioEssays
Pancreatic β‐cells in the islet of Langerhans produce the hormone insulin, which maintains blood glucose homeostasis. Perturbations in β‐cell function may lead to impairment of insulin production and secretion and the onset of diabetes mellitus. Several essential β‐cell factors have been identified that are required for normal β‐cell function, including six genes that when mutated give rise to inherited forms of diabetes known as Maturity Onset Diabetes of the Young (MODY). However, the… 
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The data show that glucose and IL-1β can activate signaling pathways, which control induction and repression of cytokines in pancreatic endocrine cells, and by these mechanisms, pancreatic β cells themselves may contribute to islet inflammation and their own immunological destruction in the pathogenesis of diabetes.
Unique Cellular and Mitochondrial Defects Mediate FK506-Induced Islet &bgr;-Cell Dysfunction
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Heterozygous Inactivation of the Na/Ca Exchanger Increases Glucose-Induced Insulin Release, β-Cell Proliferation, and Mass
TLDR
Downregulation of the Na/Ca exchanger leads to an increase inβ-cell function, proliferation, mass, and resistance to physiologic stress, namely to various changes in β- cell function that are opposite to the major abnormalities seen in type 2 diabetes.
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References

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TLDR
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TLDR
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TLDR
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TLDR
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