Evidence map›Paper›PMID 24598461›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2014

Neural circuitry underlying the central hypertensive action of nesfatin-1: melanocortins, corticotropin-releasing hormone, and oxytocin.

Gina L C Yosten, Willis K Samson

Abstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Oxytocin as an Anti-obesity Treatment.Frontiers in neuroscience · 2021
    Review
  7. Review
  8. Review
  9. Can Nesfatin-1 Predict Hypertension in Obese Children?Journal of clinical research in pediatric endocrinology · 2020
    Article
  10. Expression and function of nesfatin-1 are altered by stage of the estrous cycle.American journal of physiology. Regulatory, integrative and comparative physiology · 2019
    Article
  11. Review
  12. Article
  13. Hypoxia activates a neuropeptidergic pathway from the paraventricular nucleus of the hypothalamus to the nucleus tractus solitarii.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Article
  14. Current Understanding of the Role of Nesfatin-1.Journal of the Endocrine Society · 2018
    Review
  15. The Neurocircuitry of fluid satiation.Physiological reports · 2018
    Review
  16. Article
  17. 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.

Gina L C YostenDepartment of Pharmacological and Physiological Science, Saint Louis University School of Medicine, Saint Louis, Missouri gyosten@slu.edu.
Willis K SamsonDepartment of Pharmacological and Physiological Science, Saint Louis University School of Medicine, Saint Louis, Missouri.
Saint Louis University · US

Funding

PHYSIOLOGY OF THE PROLACTIN RELEASING PEPTIDESR01HL066023 · NHLBI · SAINT LOUIS UNIVERSITY · PI SAMSON, WILLIS K. · 2001 to 2010
$2.0M
NHLBI NIH HHS HL-066023
6 · The paper itself

Abstract

Nesfatin-1 is produced in the periphery and in the brain where it has been demonstrated to regulate appetite, stress hormone secretion, and cardiovascular function. The anorexigenic action of central nesfatin-1 requires recruitment of neurons producing the melanocortins and centrally projecting oxytocin (OT) and corticotropin-releasing hormone (CRH) neurons. We previously have shown that two components of this pathway, the central melanocortin and oxytocin systems, contribute to the hypertensive action of nesfatin-1 as well. We hypothesized that the cardiovascular effect of nesfatin-1 also was dependent on activation of neurons expressing CRH receptors, and that the order of activation of the melanocortin-CRH-oxytocin circuit was preserved for both the anorexigenic and hypertensive actions of the peptide. Pretreatment of male rats with the CRH-2 receptor antagonist astressin2B abrogated nesfatin-1-induced increases in mean arterial pressure (MAP). Furthermore, the hypertensive action of CRH was blocked by pretreatment with an oxytocin receptor antagonist ornithine vasotocin (OVT), indicating that the hypertensive effect of nesfatin-1 may require activation of oxytocinergic (OTergic) neurons in addition to recruitment of CRH neurons. Interestingly, we found that the hypertensive effect of α-melanocyte stimulating hormone (α-MSH) itself was not blocked by either astressin2B or OVT. These data suggest that while α-MSH-producing neurons are part of a core melanocortin-CRH-oxytocin circuit regulating food intake, and a subpopulation of melanocortin neurons activated by nesfatin-1 do mediate the hypertensive action of the peptide, α-MSH can signal independently from this circuit to increase MAP.

Indexed as

alpha-MSHAnimalsBlood PressureCalcium-Binding ProteinsCorticotropin-Releasing HormoneDisease Models, AnimalDNA-Binding ProteinsHormonesHypertensionMaleMelanocortinsMelanocyte-Stimulating HormonesNerve NetNerve Tissue ProteinsNucleobindinsOxytocinalpha-MSHastressin-2BCalcium-Binding ProteinsCorticotropin-Releasing HormoneDNA-Binding ProteinsHormonesMelanocortinsMelanocyte-Stimulating HormonesNerve Tissue ProteinsNucb1 protein, ratNucleobindinsOxytocinPeptide FragmentsPeptides, CyclicReceptors, Corticotropin-Releasing HormoneReceptors, OxytocinSHU 9119Vasotocincentral control of blood pressureCRHmelanocortinnesfatin-1oxytocin

Identifiers

PMID24598461
PMCPMC4025068
OpenAlexW2134216515

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.