PMID- 22556149
OWN - NLM
STAT- MEDLINE
DCOM- 20130227
LR  - 20181217
IS  - 1520-7560 (Electronic)
IS  - 1520-7552 (Linking)
VI  - 28
IP  - 7
DP  - 2012 Oct
TI  - Effects of glucocorticoids and exercise on pancreatic beta-cell function and 
      diabetes development.
PG  - 560-73
LID - 10.1002/dmrr.2310 [doi]
AB  - Peripheral insulin resistance and pancreatic beta-cell dysfunction are hallmark 
      characteristics of type 2 diabetes mellitus (T2DM). Several contributing factors 
      have been proposed to promote these two defects in individuals with T2DM, 
      including physical inactivity and chronic exposure to various psychosocial 
      factors that increase the body's exposure to glucocorticoids, the main stress 
      hormones in humans. Initially, beta-cells have been shown to adapt to these stimuli, 
      a phenomenon known as beta-cell 'compensation'. However, long-term exposure to these 
      physiologic and psychological stressors induces islet failure. Interestingly, 
      glucocorticoids stimulate beta-cell mass growth in parallel with promoting severe 
      insulin resistance, the former being an important adaptive response to the 
      latter. The direct relationship between glucocorticoids and beta-cell dysfunction 
      remains a controversial area of research. Elevations in circulating and/or tissue 
      specific glucocorticoids have been associated with the development of obesity and 
      T2DM in human and rodent models; however, the progression from insulin resistance 
      to overt T2DM is highly disputed with respect to the in vivo and in vitro effects 
      of glucocorticoids. Paradoxically, both intermittent physical stress and regular 
      exercise alleviate insulin resistance and help to preserve beta-cell mass, 
      potentially by lowering glucocorticoid levels. Recent studies have begun to 
      examine the mechanisms of intermittent and chronic glucocorticoid exposure and 
      regular exercise in altering beta-cell function. This review highlights recent 
      discoveries on the physiological regulation of beta-cells and diabetes development 
      in conditions of elevated glucocorticoids, regular exercise and intermittent 
      stress.
CI  - Copyright (c) 2012 John Wiley & Sons, Ltd.
FAU - Beaudry, Jacqueline L
AU  - Beaudry JL
AD  - School of Kinesiology and Health Science, York University, North York, Ontario, 
      Canada.
FAU - Riddell, Michael C
AU  - Riddell MC
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - Diabetes Metab Res Rev
JT  - Diabetes/metabolism research and reviews
JID - 100883450
RN  - 0 (Glucocorticoids)
RN  - 0 (Insulin)
SB  - IM
CIN - Diabetes Metab Res Rev. 2014 Feb;30(2):120-1. PMID: 24500990
CIN - Diabetes Metab Res Rev. 2014 Feb;30(2):122-3. PMID: 24500991
MH  - Animals
MH  - Diabetes Mellitus, Type 2/*etiology/metabolism/*physiopathology/prevention & 
      control
MH  - Disease Progression
MH  - *Exercise
MH  - Glucocorticoids/blood/*metabolism
MH  - Humans
MH  - Insulin/metabolism
MH  - Insulin Secretion
MH  - Insulin-Secreting Cells/*metabolism
MH  - Motor Activity
MH  - *Stress, Physiological
MH  - Stress, Psychological/blood/metabolism/*physiopathology
EDAT- 2012/05/05 06:00
MHDA- 2013/02/28 06:00
CRDT- 2012/05/05 06:00
PHST- 2012/05/05 06:00 [entrez]
PHST- 2012/05/05 06:00 [pubmed]
PHST- 2013/02/28 06:00 [medline]
AID - 10.1002/dmrr.2310 [doi]
PST - ppublish
SO  - Diabetes Metab Res Rev. 2012 Oct;28(7):560-73. doi: 10.1002/dmrr.2310.