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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 Diabetes Care 37(6). p.1751-1758
Abstract
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... (More)
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. (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
Diabetes Care
volume
37
issue
6
pages
1751 - 1758
publisher
American Diabetes Association
external identifiers
  • pmid:24812433
  • wos:000337746100055
  • scopus:84901445280
ISSN
1935-5548
DOI
10.2337/dc14-0396
language
English
LU publication?
yes
id
7adfab1c-84a1-4dfc-9ca5-7d9673b9faf3 (old id 4455565)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/24812433?dopt=Abstract
date added to LUP
2014-06-03 22:27:54
date last changed
2017-11-05 03:19:49
@article{7adfab1c-84a1-4dfc-9ca5-7d9673b9faf3,
  abstract     = {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.},
  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         = {1935-5548},
  language     = {eng},
  number       = {6},
  pages        = {1751--1758},
  publisher    = {American Diabetes Association},
  series       = {Diabetes Care},
  title        = {β-Cell Failure in Type 2 Diabetes: Postulated Mechanisms and Prospects for Prevention and Treatment.},
  url          = {http://dx.doi.org/10.2337/dc14-0396},
  volume       = {37},
  year         = {2014},
}