PMID- 25805757
OWN - NLM
STAT- MEDLINE
DCOM- 20150522
LR  - 20220321
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Linking)
VI  - 64
IP  - 4
DP  - 2015 Apr
TI  - Determinants of shortened, disrupted, and mistimed sleep and associated metabolic 
      health consequences in healthy humans.
PG  - 1073-80
LID - 10.2337/db14-1475 [doi]
AB  - Recent increases in the prevalence of obesity and type 2 diabetes mellitus (T2DM) 
      in modern societies have been paralleled by reductions in the time their denizens 
      spend asleep. Epidemiological studies have shown that disturbed sleep-comprising 
      short, low-quality, and mistimed sleep-increases the risk of metabolic diseases, 
      especially obesity and T2DM. Supporting a causal role of disturbed sleep, 
      experimental animal and human studies have found that sleep loss can impair 
      metabolic control and body weight regulation. Possible mechanisms for the 
      observed changes comprise sleep loss-induced changes in appetite-signaling 
      hormones (e.g., higher levels of the hunger-promoting hormone ghrelin) or hedonic 
      brain responses, altered responses of peripheral tissues to metabolic signals, 
      and changes in energy intake and expenditure. Even though the overall consensus 
      is that sleep loss leads to metabolic perturbations promoting the development of 
      obesity and T2DM, experimental evidence supporting the validity of this view has 
      been inconsistent. This Perspective aims at discussing molecular to behavioral 
      factors through which short, low-quality, and mistimed sleep may threaten 
      metabolic public health. In this context, possible factors that may determine the 
      extent to which poor sleep patterns increase the risk of metabolic pathologies 
      within and across generations will be discussed (e.g., timing and genetics).
CI  - (c) 2015 by the American Diabetes Association. Readers may use this article as long 
      as the work is properly cited, the use is educational and not for profit, and the 
      work is not altered.
FAU - Cedernaes, Jonathan
AU  - Cedernaes J
AD  - Department of Neuroscience, Uppsala University, Uppsala, Sweden 
      jonathan.cedernaes@neuro.uu.se.
FAU - Schioth, Helgi B
AU  - Schioth HB
AD  - Department of Neuroscience, Uppsala University, Uppsala, Sweden.
FAU - Benedict, Christian
AU  - Benedict C
AD  - Department of Neuroscience, Uppsala University, Uppsala, Sweden.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
SB  - IM
MH  - Diabetes Mellitus, Type 2/etiology/*metabolism
MH  - Female
MH  - Humans
MH  - Male
MH  - Obesity/etiology/*metabolism
MH  - Sleep Deprivation/complications/*metabolism
EDAT- 2015/03/26 06:00
MHDA- 2015/05/23 06:00
CRDT- 2015/03/26 06:00
PHST- 2015/03/26 06:00 [entrez]
PHST- 2015/03/26 06:00 [pubmed]
PHST- 2015/05/23 06:00 [medline]
AID - 64/4/1073 [pii]
AID - 10.2337/db14-1475 [doi]
PST - ppublish
SO  - Diabetes. 2015 Apr;64(4):1073-80. doi: 10.2337/db14-1475.