Evidence map›Paper›PMID 36281647›Full record

ArticleeLife2022

Oxytocin signaling in the posterior hypothalamus prevents hyperphagic obesity in mice.

Kengo Inada, Kazoku Tsujimoto, Masahide Yoshida, Katsuhiko Nishimori, Kazunari Miyamichi

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

20 citing papers in PubMed, 40 citations in OpenAlex.

  1. Effects of obesity on brain health and cognition.Nature reviews. Neurology · 2026
    Review
  2. Role of Oxytocin in Obesity.Current diabetes reports · 2026
    Review
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  10. Science translational medicine · 2025
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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

5 authors at 4 institutions in 1 country.

Kengo InadaRIKEN Center for Biosystems Dynamics Research, Kobe, Japan.ORCID 0000-0002-0859-4582
Kazoku TsujimotoRIKEN Center for Biosystems Dynamics Research, Kobe, Japan.
Masahide YoshidaLaboratory of Molecular Biology, Department of Molecular and Cell Biology, Graduate School of Agricultural Science, Tohoku University, Sendai, Japan.ORCID 0000-0003-1247-2294
Katsuhiko NishimoriLaboratory of Molecular Biology, Department of Molecular and Cell Biology, Graduate School of Agricultural Science, Tohoku University, Sendai, Japan.
Kazunari MiyamichiRIKEN Center for Biosystems Dynamics Research, Kobe, Japan.ORCID 0000-0002-7807-8436
RIKEN Center for Biosystems Dynamics Research · JPFukushima Medical University · JPJapan Science and Technology Agency · JPJichi Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Decades of studies have revealed molecular and neural circuit bases for body weight homeostasis. Neural hormone oxytocin (Oxt) has received attention in this context because it is produced by neurons in the paraventricular hypothalamic nucleus (PVH), a known output center of hypothalamic regulation of appetite. Oxt has an anorexigenic effect, as shown in human studies, and can mediate satiety signals in rodents. However, the function of Oxt signaling in the physiological regulation of appetite has remained in question, because whole-body knockout (KO) of

Indexed as

LeptinOxytocinAnimalsBody WeightHumansHyperphagiaHypothalamusHypothalamus, PosteriorMiceObesityParaventricular Hypothalamic NucleusTriglyceridesLeptinOxytocinTriglyceridesconditional knockoutgeneticsgenomicshyperphagic obesityleptinmouseneuroscienceoxytocinoxytocin receptor

Identifiers

PMID36281647
PMCPMC9596155
OpenAlexW4306976414

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.