PMID- 21099255
OWN - NLM
STAT- MEDLINE
DCOM- 20110331
LR  - 20141009
IS  - 1938-2022 (Electronic)
IS  - 1938-2014 (Linking)
VI  - 1
IP  - 2
DP  - 2009 Sep-Oct
TI  - The role of insulin signaling in the development of beta-cell dysfunction and 
      diabetes.
PG  - 95-101
LID - 10.4161/isl.1.2.9263 [doi]
AB  - The peptide hormone insulin not only regulates metabolic pathways, but also 
      proliferative signaling pathways. Insulin regulates cell proliferation, protein 
      synthesis and gene expression in most, if not all, mammalian tissues. Extensive 
      recent studies have shown that insulin also plays an important role in the 
      regulation of pancreatic islet beta-cell function. In the development of peripheral 
      insulin resistance leading to an increased demand for insulin production, 
      increase in beta-cell mass by compensatory hyperplasia and hypertrophy of beta-cells 
      and insulin output is a crucial mechanism to maintain euglycemia. Indeed, 
      impaired insulin signaling in the beta-cells and increased beta-cell apoptosis are 
      associated with the onset of diabetes in obese insulin resistant type 2 diabetes 
      mellitus (T2DM). Studies using gene knockout approaches in mice have further 
      demonstrated that the insulin signaling in the beta-cells is critical for mediating 
      insulin action on them to maintain appropriate mass and insulin production. It is 
      conceivable that insulin resistance, which is usually associated with the 
      compensatory mechanism of hyperinsulinemia, occurring in the beta-cells could be a 
      major contributor leading to increased rate of beta-cell death and declined beta-cell 
      mass. It is hypothesized that a strategy to improve intra-islet insulin action 
      via enhancing beta-cell responsiveness could be a considerable benefit in the 
      prevention and treatment of T2DM.
FAU - Wang, Qinghua
AU  - Wang Q
AD  - Division of Endocrinology and Metabolism, Li Ka-Shing Knowledge Institute, St. 
      Michael's Hospital, Toronto, Ontario, Canada. qinghua.wang@utoronto.ca
FAU - Jin, Tianru
AU  - Jin T
LA  - eng
GR  - Canadian Institutes of Health Research/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - Islets
JT  - Islets
JID - 101495366
RN  - 0 (Insulin)
SB  - IM
MH  - Animals
MH  - Diabetes Complications/metabolism/physiopathology
MH  - Diabetes Mellitus/metabolism/*physiopathology
MH  - Hyperglycemia/etiology/metabolism/pathology
MH  - Insulin/metabolism/*physiology
MH  - Insulin-Secreting Cells/metabolism/pathology/*physiology
MH  - Mice
MH  - Models, Biological
MH  - Organ Size/physiology
MH  - Signal Transduction/physiology
EDAT- 2009/09/01 00:00
MHDA- 2011/04/01 06:00
CRDT- 2010/11/25 06:00
PHST- 2010/11/25 06:00 [entrez]
PHST- 2009/09/01 00:00 [pubmed]
PHST- 2011/04/01 06:00 [medline]
AID - 9263 [pii]
AID - 10.4161/isl.1.2.9263 [doi]
PST - ppublish
SO  - Islets. 2009 Sep-Oct;1(2):95-101. doi: 10.4161/isl.1.2.9263.