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β-cell Failure in Type 2 Diabetes: Postulated Mechanisms and Prospects for Prevention and Treatment.

Halban, Philippe A; Polonsky, Kenneth S; Bowden, Donald W; Hawkins, Meredith A; Ling, Charlotte LU ; Mather, Kieren J; Powers, Alvin C; Rhodes, Christopher J; Sussel, Lori and Weir, Gordon C (2014) In Journal of Clinical Endocrinology and Metabolism 99(6). p.1983-1992
Abstract
Objective: This report examines the foundation of β-cell failure in type 2 diabetes and suggests areas for future research on the underlying mechanisms that may lead to improved prevention and treatment. Participants: A group of experts participated in a conference on October 14-16, 2013 cosponsored by The Endocrine Society and the American Diabetes Association. A writing group prepared this summary and recommendations. Evidence: The writing group based this report on conference presentations, discussion, and debate. Topics covered include genetic predisposition, the 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... (More)
Objective: This report examines the foundation of β-cell failure in type 2 diabetes and suggests areas for future research on the underlying mechanisms that may lead to improved prevention and treatment. Participants: A group of experts participated in a conference on October 14-16, 2013 cosponsored by The Endocrine Society and the American Diabetes Association. A writing group prepared this summary and recommendations. Evidence: The writing group based this report on conference presentations, discussion, and debate. Topics covered include genetic predisposition, the 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 type 2 diabetes. 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: 1) Impact the natural history of β-cell failure; 2) Identify and characterize genetic loci for type 2 diabetes; 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; 7) Identify circulating factors and neuronal circuits underlying the axis of communication between the brain and β-cells. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Clinical Endocrinology and Metabolism
volume
99
issue
6
pages
1983 - 1992
publisher
The Endocrine Society
external identifiers
  • wos:000342340500037
  • pmid:24712577
  • scopus:84902352296
ISSN
1945-7197
DOI
10.1210/jc.2014-1425
language
English
LU publication?
yes
id
94843db3-af97-4347-9d23-d14553462253 (old id 4430637)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/24712577?dopt=Abstract
date added to LUP
2014-05-06 19:20:16
date last changed
2017-11-05 03:09:02
@article{94843db3-af97-4347-9d23-d14553462253,
  abstract     = {Objective: This report examines the foundation of β-cell failure in type 2 diabetes and suggests areas for future research on the underlying mechanisms that may lead to improved prevention and treatment. Participants: A group of experts participated in a conference on October 14-16, 2013 cosponsored by The Endocrine Society and the American Diabetes Association. A writing group prepared this summary and recommendations. Evidence: The writing group based this report on conference presentations, discussion, and debate. Topics covered include genetic predisposition, the 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 type 2 diabetes. 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: 1) Impact the natural history of β-cell failure; 2) Identify and characterize genetic loci for type 2 diabetes; 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; 7) Identify circulating factors and neuronal circuits underlying the axis of communication between the brain and β-cells.},
  author       = {Halban, Philippe A and Polonsky, Kenneth S and Bowden, Donald W and Hawkins, Meredith A and Ling, Charlotte and Mather, Kieren J and Powers, Alvin C and Rhodes, Christopher J and Sussel, Lori and Weir, Gordon C},
  issn         = {1945-7197},
  language     = {eng},
  number       = {6},
  pages        = {1983--1992},
  publisher    = {The Endocrine Society},
  series       = {Journal of Clinical Endocrinology and Metabolism},
  title        = {β-cell Failure in Type 2 Diabetes: Postulated Mechanisms and Prospects for Prevention and Treatment.},
  url          = {http://dx.doi.org/10.1210/jc.2014-1425},
  volume       = {99},
  year         = {2014},
}