PMID- 24532160
OWN - NLM
STAT- MEDLINE
DCOM- 20141118
LR  - 20211021
IS  - 1539-0829 (Electronic)
IS  - 1534-4827 (Print)
IS  - 1534-4827 (Linking)
VI  - 14
IP  - 4
DP  - 2014 Apr
TI  - Does disruption of circadian rhythms contribute to beta-cell failure in type 2 
      diabetes?
PG  - 474
LID - 10.1007/s11892-014-0474-4 [doi]
AB  - Type 2 diabetes mellitus (T2DM) is a complex metabolic disease characterized by 
      the loss of beta-cell secretory function and mass. The pathophysiology of 
      beta-cell failure in T2DM involves a complex interaction between genetic 
      susceptibilities and environmental risk factors. One environmental condition that 
      is gaining greater appreciation as a risk factor for T2DM is the disruption of 
      circadian rhythms (eg, shift-work and sleep loss). In recent years, circadian 
      disruption has become increasingly prevalent in modern societies and consistently 
      shown to augment T2DM susceptibility (partly mediated through its effects on 
      pancreatic beta-cells). Since beta-cell failure is essential for development of 
      T2DM, we will review current work from epidemiologic, clinical, and animal 
      studies designed to gain insights into the molecular and physiological mechanisms 
      underlying the predisposition to beta-cell failure associated with circadian 
      disruption. Elucidating the role of circadian clocks in regulating beta-cell 
      health will add to our understanding of T2DM pathophysiology and may contribute 
      to the development of novel therapeutic and preventative approaches.
FAU - Rakshit, Kuntol
AU  - Rakshit K
AD  - Larry L. Hillblom Islet Research Center, Department of Medicine, Division of 
      Endocrinology, University of California Los Angeles, David Geffen School of 
      Medicine, Los Angeles, California, 900A Weyburn Place, Los Angeles, CA, 90095, 
      USA.
FAU - Thomas, Anthony P
AU  - Thomas AP
FAU - Matveyenko, Aleksey V
AU  - Matveyenko AV
LA  - eng
GR  - R01 DK098468/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Curr Diab Rep
JT  - Current diabetes reports
JID - 101093791
RN  - 0 (Blood Glucose)
SB  - IM
MH  - Animals
MH  - Blood Glucose/*metabolism
MH  - Circadian Clocks
MH  - *Circadian Rhythm
MH  - Diabetes Mellitus, Type 2/etiology/metabolism/*physiopathology
MH  - Employment
MH  - Endoplasmic Reticulum Stress
MH  - Environmental Exposure
MH  - Female
MH  - Genetic Predisposition to Disease
MH  - Humans
MH  - Inflammation/metabolism
MH  - *Insulin Resistance
MH  - Insulin-Secreting Cells/*metabolism
MH  - Male
MH  - Oxidative Stress
PMC - PMC3988110
MID - NIHMS568115
COIS- Conflict of Interest Kuntol Rakshit declares that he has no conflict of interest. 
      Anthony P. Thomas declares that he has no conflict of interest. Aleksey V. 
      Matveyenko declares that he has no conflict of interest.
EDAT- 2014/02/18 06:00
MHDA- 2014/11/19 06:00
PMCR- 2014/04/15
CRDT- 2014/02/18 06:00
PHST- 2014/02/18 06:00 [entrez]
PHST- 2014/02/18 06:00 [pubmed]
PHST- 2014/11/19 06:00 [medline]
PHST- 2014/04/15 00:00 [pmc-release]
AID - 10.1007/s11892-014-0474-4 [doi]
PST - ppublish
SO  - Curr Diab Rep. 2014 Apr;14(4):474. doi: 10.1007/s11892-014-0474-4.