PMID- 23775768
OWN - NLM
STAT- MEDLINE
DCOM- 20131210
LR  - 20220317
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Print)
IS  - 0012-1797 (Linking)
VI  - 62
IP  - 10
DP  - 2013 Oct
TI  - Consequences of exposure to light at night on the pancreatic islet circadian 
      clock and function in rats.
PG  - 3469-78
LID - 10.2337/db12-1543 [doi]
AB  - There is a correlation between circadian disruption, type 2 diabetes mellitus 
      (T2DM), and islet failure. However, the mechanisms underlying this association 
      are largely unknown. Pancreatic islets express self-sustained circadian clocks 
      essential for proper beta-cell function and survival. We hypothesized that exposure 
      to environmental conditions associated with disruption of circadian rhythms and 
      susceptibility to T2DM in humans disrupts islet clock and beta-cell function. To 
      address this hypothesis, we validated the use of Per-1:LUC transgenic rats for 
      continuous longitudinal assessment of islet circadian clock function ex vivo. 
      Using this methodology, we subsequently examined effects of the continuous 
      exposure to light at night (LL) on islet circadian clock and insulin secretion in 
      vitro in rat islets. Our data show that changes in the light-dark cycle in vivo 
      entrain the phase of islet clock transcriptional oscillations, whereas prolonged 
      exposure (10 weeks) to LL disrupts islet circadian clock function through 
      impairment in the amplitude, phase, and interislet synchrony of clock 
      transcriptional oscillations. We also report that exposure to LL leads to 
      diminished glucose-stimulated insulin secretion due to a decrease in insulin 
      secretory pulse mass. Our studies identify potential mechanisms by which 
      disturbances in circadian rhythms common to modern life can predispose to islet 
      failure in T2DM.
FAU - Qian, Jingyi
AU  - Qian J
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.
FAU - Block, Gene D
AU  - Block GD
FAU - Colwell, Christopher S
AU  - Colwell CS
FAU - Matveyenko, Aleksey V
AU  - Matveyenko AV
LA  - eng
GR  - K01 DK089003/DK/NIDDK NIH HHS/United States
GR  - R01 DK098468/DK/NIDDK NIH HHS/United States
GR  - K01DK089003/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20130617
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
RN  - 0 (Blood Glucose)
RN  - 0 (Per1 protein, rat)
RN  - 0 (Period Circadian Proteins)
RN  - EC 2.3.1.48 (CLOCK Proteins)
SB  - IM
MH  - Animals
MH  - Blood Glucose/metabolism
MH  - Body Weight
MH  - CLOCK Proteins/*metabolism
MH  - *Circadian Clocks
MH  - *Circadian Rhythm
MH  - Diabetes Mellitus, Experimental/*metabolism/physiopathology
MH  - Diabetes Mellitus, Type 2/*metabolism/physiopathology
MH  - Disease Susceptibility
MH  - Immunohistochemistry
MH  - Insulin-Secreting Cells/metabolism
MH  - Islets of Langerhans/metabolism
MH  - *Light
MH  - Motor Activity
MH  - Period Circadian Proteins/*metabolism
MH  - Rats
MH  - Rats, Transgenic
PMC - PMC3781472
EDAT- 2013/06/19 06:00
MHDA- 2013/12/16 06:00
PMCR- 2014/10/01
CRDT- 2013/06/19 06:00
PHST- 2013/06/19 06:00 [entrez]
PHST- 2013/06/19 06:00 [pubmed]
PHST- 2013/12/16 06:00 [medline]
PHST- 2014/10/01 00:00 [pmc-release]
AID - db12-1543 [pii]
AID - 1543 [pii]
AID - 10.2337/db12-1543 [doi]
PST - ppublish
SO  - Diabetes. 2013 Oct;62(10):3469-78. doi: 10.2337/db12-1543. Epub 2013 Jun 17.