β-cell failure in type 2 diabetes: postulated mechanisms and prospects for prevention and treatment

dc.contributor.authorHalban, Philippe A.
dc.contributor.authorPolonsky, Kenneth S.
dc.contributor.authorBowden, Donald W.
dc.contributor.authorHawkins, Meredith A.
dc.contributor.authorLing, Charlotte
dc.contributor.authorMather, Kieren J.
dc.contributor.authorPowers, Alvin C.
dc.contributor.authorRhodes, Christopher J.
dc.contributor.authorSussel, Lori
dc.contributor.authorWeir, Gordon C.
dc.contributor.departmentMedicine, School of Medicineen_US
dc.date.accessioned2020-02-06T20:02:09Z
dc.date.available2020-02-06T20:02:09Z
dc.date.issued2014-06
dc.description.abstractOBJECTIVE: This article examines the foundation of β-cell failure in type 2 diabetes (T2D) and suggests areas for future research on the underlying mechanisms that may lead to improved prevention and treatment. RESEARCH DESIGN AND METHODS: A group of experts participated in a conference on 14-16 October 2013 cosponsored by the Endocrine Society and the American Diabetes Association. A writing group prepared this summary and recommendations. RESULTS: The writing group based this article on conference presentations, discussion, and debate. Topics covered include genetic predisposition, foundations of β-cell failure, natural history of β-cell failure, and impact of therapeutic interventions. CONCLUSIONS: β-Cell failure is central to the development and progression of T2D. It antedates and predicts diabetes onset and progression, is in part genetically determined, and often can be identified with accuracy even though current tests are cumbersome and not well standardized. Multiple pathways underlie decreased β-cell function and mass, some of which may be shared and may also be a consequence of processes that initially caused dysfunction. Goals for future research include to 1) impact the natural history of β-cell failure; 2) identify and characterize genetic loci for T2D; 3) target β-cell signaling, metabolic, and genetic pathways to improve function/mass; 4) develop alternative sources of β-cells for cell-based therapy; 5) focus on metabolic environment to provide indirect benefit to β-cells; 6) improve understanding of the physiology of responses to bypass surgery; and 7) identify circulating factors and neuronal circuits underlying the axis of communication between the brain and β-cells.en_US
dc.identifier.citationHalban, P. A., Polonsky, K. S., Bowden, D. W., Hawkins, M. A., Ling, C., Mather, K. J., … Weir, G. C. (2014). β-cell failure in type 2 diabetes: postulated mechanisms and prospects for prevention and treatment. The Journal of clinical endocrinology and metabolism, 99(6), 1983–1992. doi:10.1210/jc.2014-1425en_US
dc.identifier.urihttps://hdl.handle.net/1805/22016
dc.language.isoen_USen_US
dc.publisherEndocrine Societyen_US
dc.relation.isversionof10.1210/jc.2014-1425en_US
dc.relation.journalThe Journal of Clinical Endocrinology and Metabolismen_US
dc.rightsPublisher Policyen_US
dc.sourcePMCen_US
dc.subjectCell deathen_US
dc.subjectCell dedifferentiationen_US
dc.subjectDiabetes Mellitus, Type 2en_US
dc.subjectEndoplasmic Reticulum Stressen_US
dc.subjectEpigenesis, Geneticen_US
dc.subjectInflammationen_US
dc.subjectInsulin-Secreting Cellsen_US
dc.titleβ-cell failure in type 2 diabetes: postulated mechanisms and prospects for prevention and treatmenten_US
dc.typeArticleen_US
ul.alternative.fulltexthttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5393482/en_US
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