alpha Cell Function and Gene Expression Are Compromised in Type 1 Diabetes
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UMass Chan Affiliations
Department of Medicine, Diabetes Division, Diabetes Center of ExcellenceDocument Type
Journal ArticlePublication Date
2018-03-06Keywords
alpha cellsglucagon
human
insulin
pancreatic islet
type 1 diabetes
Cell Biology
Cellular and Molecular Physiology
Endocrine System Diseases
Endocrinology
Genetic Phenomena
Hormones, Hormone Substitutes, and Hormone Antagonists
Immune System Diseases
Nutritional and Metabolic Diseases
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Many patients with type 1 diabetes (T1D) have residual beta cells producing small amounts of C-peptide long after disease onset but develop an inadequate glucagon response to hypoglycemia following T1D diagnosis. The features of these residual beta cells and alpha cells in the islet endocrine compartment are largely unknown, due to the difficulty of comprehensive investigation. By studying the T1D pancreas and isolated islets, we show that remnant beta cells appeared to maintain several aspects of regulated insulin secretion. However, the function of T1D alpha cells was markedly reduced, and these cells had alterations in transcription factors constituting alpha and beta cell identity. In the native pancreas and after placing the T1D islets into a non-autoimmune, normoglycemic in vivo environment, there was no evidence of alpha-to-beta cell conversion. These results suggest an explanation for the disordered T1D counterregulatory glucagon response to hypoglycemia.Source
Cell Rep. 2018 Mar 6;22(10):2667-2676. doi: 10.1016/j.celrep.2018.02.032. Link to article on publisher's site
DOI
10.1016/j.celrep.2018.02.032Permanent Link to this Item
http://hdl.handle.net/20.500.14038/40610PubMed ID
29514095Notes
Full author list omitted for brevity. For the full list of authors, see article.
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© 2018 The Authors. Under a Creative Commons license: Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)Distribution License
http://creativecommons.org/licenses/by-nc-nd/4.0/ae974a485f413a2113503eed53cd6c53
10.1016/j.celrep.2018.02.032
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Except where otherwise noted, this item's license is described as © 2018 The Authors. Under a Creative Commons license: Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)