Evidence map›Paper›PMID 19506316›Full record

ReviewILAR journal2009

Metabolic consequences of sleep-disordered breathing.

Jonathan Jun, Vsevolod Y Polotsky

Open access · bronzeAbstract readReview
In one paragraph

Review in ILAR journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
6.2field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

44 citing papers in PubMed, 102 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Article
  7. Endothelin-1 as a novel target for the prevention of metabolic dysfunction with intermittent hypoxia in male participants.American journal of physiology. Regulatory, integrative and comparative physiology · 2022
    Article
  8. Sleep Apnea and Cardiovascular Disease.Current diabetes reports · 2021
    Review
  9. Role of obstructive sleep apnea in metabolic risk in PCOS.Current opinion in endocrine and metabolic research · 2021
    Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Stressful sleep.The European respiratory journal · 2016
    Article
  19. Article
  20. Inflammation in sleep apnea: an update.Reviews in endocrine & metabolic disorders · 2015
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Jonathan JunDivision of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21224, USA. jjun2@jhmi.edu
Vsevolod Y Polotsky
Johns Hopkins University · US

Funding

MULTIDISCIPLINARY TRAINING PROGRAM IN LUNG DISEASEST32HL007534 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI Nadia N Hansel, Larissa A. Shimoda · 1985 to 2026
$28.3M
Sleep Related Mechanisms of COPD ProgressionP50HL084945 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BROWN, ROBERT H · 2007 to 2011
$15.1M
Sleep Apnea and Dysregulation of Lipid MetabolismR01HL080105 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI POLOTSKY, VSEVOLOD Y · 2005 to 2014
$3.4M
Mechanisms and Consequences of Intermittent Hypoxia-Induced LipolysisK08HL109475 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI JUN, JONATHAN C. · 2012 to 2016
$725k
NHLBI NIH HHS 5P50HL084945NHLBI NIH HHS K08 HL109475NHLBI NIH HHS P50 HL084945NHLBI NIH HHS R01 HL080105NHLBI NIH HHS R01 HL80105NHLBI NIH HHS T32 HL007534NHLBI NIH HHS T32 HL07534
6 · The paper itself

Abstract

There is increasing evidence of a causal relationship between sleep-disordered breathing and metabolic dysfunction. Metabolic syndrome (MetS), a cluster of risk factors that promote atherosclerotic cardiovascular disease, comprises central obesity, insulin resistance, glucose intolerance, dyslipidemia, and hypertension, manifestations of altered total body energy regulation. Excess caloric intake is indisputably the key driver of MetS, but other environmental and genetic factors likely play a role; in particular, obstructive sleep apnea (OSA), characterized by intermittent hypoxia (IH), may induce or exacerbate various aspects of MetS. Clinical studies show that OSA can affect glucose metabolism, cholesterol, inflammatory markers, and nonalcoholic fatty liver disease. Animal models of OSA enable scientists to circumvent confounders such as obesity in clinical studies. In the most widely used model, which involves exposing rodents to IH during their sleep phase, the IH alters circadian glucose homeostasis, impairs muscle carbohydrate uptake, induces hyperlipidemia, and upregulates cholesterol synthesis enzymes. Complicating factors such as obesity or a high-fat diet lead to progressive insulin resistance and liver inflammation, respectively. Mechanisms for these effects are not yet fully understood, but are likely related to energy-conserving adaptations to hypoxia, which is a strong catabolic stressor. Finally, IH may contribute to the morbidity of MetS by inducing inflammation and oxidative stress. Identification of OSA as a potential causative factor in MetS would have immense clinical impact and could improve the management and understanding of both disorders.

Indexed as

AnimalsDyslipidemiasHumansHypoxiaLiver DiseasesMetabolic DiseasesMiceObesityRatsSleep Apnea SyndromesSleep Deprivation

Identifiers

PMID19506316
PMCPMC5689472
OpenAlexW2166022644

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.