Evidence map›Paper›PMID 36302800›Full record

ArticleScientific reports2022

Neuromedin U-deficient rats do not lose body weight or food intake.

Kyoka Yokogi, Yuki Goto, Mai Otsuka, Fumiya Ojima, Tomoe Kobayashi, Yukina Tsuchiba, Yu Takeuchi, Masumi Namba, Mayumi Kohno, Minami Tetsuka and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.8field-weighted citation impact, top 33% 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

2 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. 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

13 authors at 3 institutions in 1 country.

Kyoka YokogiDepartment of Biology, Graduate School of Natural Science and Technology, Okayama University, 3-1-1 Tsushimanaka, Kitaku, Okayama, 700-8530, Japan.
Yuki GotoDepartment of Biology, Graduate School of Natural Science and Technology, Okayama University, 3-1-1 Tsushimanaka, Kitaku, Okayama, 700-8530, Japan.
Mai OtsukaDepartment of Biology, Graduate School of Natural Science and Technology, Okayama University, 3-1-1 Tsushimanaka, Kitaku, Okayama, 700-8530, Japan.
Fumiya OjimaDepartment of Natural Sciences and Biology, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama, 701-0192, Japan.
Tomoe KobayashiDivision of Molecular Genetics, Shigei Medical Research Institute, 2117 Yamada, Minami-ku, Okayama, 701-0202, Japan.
Yukina TsuchibaDepartment of Biology, Graduate School of Natural Science and Technology, Okayama University, 3-1-1 Tsushimanaka, Kitaku, Okayama, 700-8530, Japan.
Yu TakeuchiDepartment of Biology, Graduate School of Natural Science and Technology, Okayama University, 3-1-1 Tsushimanaka, Kitaku, Okayama, 700-8530, Japan.
Masumi NambaDivision of Molecular Genetics, Shigei Medical Research Institute, 2117 Yamada, Minami-ku, Okayama, 701-0202, Japan.
Mayumi KohnoDivision of Molecular Genetics, Shigei Medical Research Institute, 2117 Yamada, Minami-ku, Okayama, 701-0202, Japan.
Minami TetsukaDepartment of Biology, Graduate School of Natural Science and Technology, Okayama University, 3-1-1 Tsushimanaka, Kitaku, Okayama, 700-8530, Japan.
Sakae TakeuchiDepartment of Biology, Graduate School of Natural Science and Technology, Okayama University, 3-1-1 Tsushimanaka, Kitaku, Okayama, 700-8530, Japan.
Makoto Matsuyama *Division of Molecular Genetics, Shigei Medical Research Institute, 2117 Yamada, Minami-ku, Okayama, 701-0202, Japan. matsuyama@shigei.or.jp.
Sayaka Aizawa *Department of Biology, Graduate School of Natural Science and Technology, Okayama University, 3-1-1 Tsushimanaka, Kitaku, Okayama, 700-8530, Japan. saizawa@okayama-u.ac.jp.
Okayama University · JPShigei Medical Research Institute · JPKawasaki Medical School · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Studies in genetically modified mice establish that essential roles of endogenous neuromedin U (NMU) are anorexigenic function and metabolic regulation, indicating that NMU is expected to be a potential target for anti-obesity agents. However, in central administration experiments in rats, inconsistent results have been obtained, and the essential role of NMU energy metabolism in rats remain unclear. This study aims to elucidate the role of endogenous NMU in rats. We generated NMU knockout (KO) rats that unexpectedly showed no difference in body weight, adiposity, circulating metabolic markers, body temperature, locomotor activity, and food consumption in both normal and high fat chow feeding. Furthermore, unlike reported in mice, expressions of Nmu and NMU receptor type 2 (Nmur2) mRNA were hardly detectable in the rat hypothalamic nuclei regulating feeding and energy metabolism, including the arcuate nucleus and paraventricular nucleus, while Nmu was expressed in pars tuberalis and Nmur2 was expressed in the ependymal cell layer of the third ventricle. These results indicate that the species-specific expression pattern of Nmu and Nmur2 may allow NMU to have distinct functions across species, and that endogenous NMU does not function as an anorexigenic hormone in rats.

Indexed as

NeuropeptidesPeptide HormonesAnimalsBody WeightEatingMiceRatsReceptors, Neurotransmitterneuromedin UNeuropeptidesPeptide HormonesReceptors, Neurotransmitter

Identifiers

PMID36302800
PMCPMC9614009
OpenAlexW4307645515

What OpenQuestion holds

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LicenceCC BY
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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.