Evidence map›Paper›PMID 26095748›Full record

ReviewThe Journal of physiology2016

Facilitation of breathing by leptin effects in the central nervous system.

M Bassi, W I Furuya, D B Zoccal, J V Menani, D S A Colombari, D K Mulkey, E Colombari

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-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

16 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Observational
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Obstructive sleep apnea.Handbook of clinical neurology · 2022
    Review
  10. Article
  11. Review
  12. Article
  13. Intranasal Leptin Prevents Opioid-induced Sleep-disordered Breathing in Obese Mice.American journal of respiratory cell and molecular biology · 2020
    Article
  14. Article
  15. Article
  16. Article
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

7 authors at 2 institutions in 2 countries.

M BassiDepartment of Physiology and Pathology, School of Dentistry, São Paulo State University (UNESP), Araraquara, SP, Brazil.
W I FuruyaDepartment of Physiology and Pathology, School of Dentistry, São Paulo State University (UNESP), Araraquara, SP, Brazil.
D B ZoccalDepartment of Physiology and Pathology, School of Dentistry, São Paulo State University (UNESP), Araraquara, SP, Brazil.
J V MenaniDepartment of Physiology and Pathology, School of Dentistry, São Paulo State University (UNESP), Araraquara, SP, Brazil.
D S A ColombariDepartment of Physiology and Pathology, School of Dentistry, São Paulo State University (UNESP), Araraquara, SP, Brazil.
D K MulkeyDepartment of Physiology and Neurobiology, University of Connecticut, Storrs, CT, USA.
E ColombariDepartment of Physiology and Pathology, School of Dentistry, São Paulo State University (UNESP), Araraquara, SP, Brazil.
Universidade Estadual Paulista (Unesp) · BRUniversity of Connecticut · US

Funding

Glial chemosensitivity: pH sensing and interactions with neuronal chemoreceptorsR01HL104101 · NHLBI · UNIVERSITY OF CONNECTICUT STORRS · PI MULKEY, DANIEL K, OLSEN, MICHELLE L · 2010 to 2024
$5.5M
CRCNS: Modeling the respiratory-sympathetic coupling in neurogenic hypertensionR01AT008632 · NCCIH · INDIANA UNIVERSITY INDIANAPOLIS · PI MOLKOV, YAROSLAV · 2015 to 2019
$1.4M
NCCIH NIH HHS R01 AT008632NHLBI NIH HHS HL104101
6 · The paper itself

Abstract

With the global epidemic of obesity, breathing disorders associated with excess body weight have markedly increased. Respiratory dysfunctions caused by obesity were originally attributed to mechanical factors; however, recent studies have suggested a pathophysiological component that involves the central nervous system (CNS) and hormones such as leptin produced by adipocytes as well as other cells. Leptin is suggested to stimulate breathing and leptin deficiency causes an impairment of the chemoreflex, which can be reverted by leptin therapy. This facilitation of the chemoreflex may depend on the action of leptin in the hindbrain areas involved in the respiratory control such as the nucleus of the solitary tract (NTS), a site that receives chemosensory afferents, and the ventral surface of the medulla that includes the retrotrapezoid nucleus (RTN), a central chemosensitive area, and the rostral ventrolateral medulla (RVLM). Although the mechanisms and pathways activated by leptin to facilitate breathing are still not completely clear, evidence suggests that the facilitatory effects of leptin on breathing require the brain melanocortin system, including the POMC-MC4R pathway, a mechanism also activated by leptin to modulate blood pressure. The results of all the studies that have investigated the effect of leptin on breathing suggest that disruption of leptin signalling as caused by obesity-induced reduction of central leptin function (leptin resistance) is a relevant mechanism that may contribute to respiratory dysfunctions associated with obesity.

Indexed as

RespirationAnimalsCentral Nervous SystemHumansLeptinObesityLeptin

Identifiers

PMID26095748
PMCPMC4799963
OpenAlexW2157559088

What OpenQuestion holds

Textmetadata
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.