Evidence map›Paper›PMID 29055392›Full record

ArticleMedical hypotheses2017

Sleep apnea: An overlooked cause of lipotoxicity?

Chenjuan Gu, Haris Younas, Jonathan C Jun

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Medical hypotheses, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

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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

3 authors at 2 institutions in 2 countries.

Chenjuan GuDivision of Pulmonary and Critical Care, Department of Medicine, Johns Hopkins University, Baltimore, MD, USA; Department of Pulmonary and Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Haris YounasDivision of Pulmonary and Critical Care, Department of Medicine, Johns Hopkins University, Baltimore, MD, USA.
Jonathan C JunDivision of Pulmonary and Critical Care, Department of Medicine, Johns Hopkins University, Baltimore, MD, USA. Electronic address: jjun2@jhmi.edu.
Johns Hopkins University · USShanghai Jiao Tong University · CN

Funding

Research BaseP30DK072488 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI MITCHELL, BRAXTON D, TAYLOR, SIMEON I. · 2005 to 2019
$17.3M
Melanocortin 4 signaling in the carotid body in obesityR01HL133100 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI Vsevolod Y Polotsky, Wan-yee Tang · 2016 to 2026
$7.1M
Treatment of Sleep Apnea by Targeting Leptin SignalingR01HL128970 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI MENDELOWITZ, DAVID, POLOTSKY, VSEVOLOD Y · 2015 to 2023
$5.4M
The role of obesity in biological responses to particulate matter in miceP50ES018176 · NIEHS · JOHNS HOPKINS UNIVERSITY · PI HANSEL, NADIA N · 2015 to 2019
$4.8M
Mechanisms and Consequences of Intermittent Hypoxia-Induced LipolysisK08HL109475 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI JUN, JONATHAN C. · 2012 to 2016
$725k
Pilot Study of Beta Adrenergic Blockade to Prevent Metabolic Consequences of Sleep ApneaR03HL138068 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI JUN, JONATHAN C. · 2017 to 2018
$164k
NHLBI NIH HHS K08 HL109475NHLBI NIH HHS R01 HL128970NHLBI NIH HHS R01 HL133100NHLBI NIH HHS R03 HL138068NIDDK NIH HHS P30 DK072488NIEHS NIH HHS P50 ES018176
6 · The paper itself

Abstract

Obstructive sleep apnea (OSA) is a common sleep disorder associated with diabetes and cardiovascular disease. However, the mechanisms by which OSA causes cardiometabolic dysfunction are not fully elucidated. OSA increases plasma free fatty acids (FFA) during sleep, reflecting excessive adipose tissue lipolysis. In animal studies, intermittent hypoxia simulating OSA also increases FFA, and the increase is attenuated by beta-adrenergic blockade. In other contexts, excessive plasma FFA can lead to ectopic fat accumulation, insulin resistance, vascular dysfunction, and dyslipidemia. Herein, we propose that OSA is a cause of excessive adipose tissue lipolysis contributing towards systemic "lipotoxicity". Since visceral and upper-body obesity contributes to OSA pathogenesis, OSA-induced lipolysis may further aggravate the consequences of this metabolically harmful state. If this hypothesis is correct, then OSA may represent a reversible risk factor for cardio-metabolic dysfunction, and this risk might be mitigated by preventing OSA-induced lipolysis during sleep.

Indexed as

LipolysisAdipose TissueAnimalsCardiovascular DiseasesDyslipidemiasFatty Acids, NonesterifiedHumansHypothalamo-Hypophyseal SystemHypoxiaInsulin ResistanceLipidsMetabolic SyndromeModels, BiologicalObesityRisk FactorsSleepFatty Acids, NonesterifiedLipidsFree fatty acidLipolysisLipotoxicitySleep apneaSympathetic nervous system

Identifiers

PMID29055392
PMCPMC5685168
OpenAlexW2754960096

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.