Evidence map›Paper›PMID 24924345›Full record

SynthesisPloS one2014

Meta-analysis of melanin-concentrating hormone signaling-deficient mice on behavioral and metabolic phenotypes.

Kenkichi Takase, Kenichi Kikuchi, Yousuke Tsuneoka, Satoko Oda, Masaru Kuroda, Hiromasa Funato

Open access · goldAbstract readMeta-Analysis
In one paragraph

Synthesis in PloS one, 2014. 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
1.9field-weighted citation impact, top 15% 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, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Optogenetic Investigation of Arousal Circuits.International journal of molecular sciences · 2017
    Review
  6. Review
  7. Article
  8. Article
  9. Optogenetic evidence for inhibitory signaling from orexin to MCH neurons via local microcircuits.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  10. Article
  11. Review
  12. 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

6 authors at 2 institutions in 1 country.

Kenkichi TakaseDepartment of Anatomy, Toho University School of Medicine, Tokyo, Japan.
Kenichi KikuchiDepartment of Information Science, Faculty of Science, Toho University, Chiba, Japan.
Yousuke TsuneokaDepartment of Anatomy, Toho University School of Medicine, Tokyo, Japan.
Satoko OdaDepartment of Anatomy, Toho University School of Medicine, Tokyo, Japan.
Masaru KurodaDepartment of Anatomy, Toho University School of Medicine, Tokyo, Japan.
Hiromasa FunatoDepartment of Anatomy, Toho University School of Medicine, Tokyo, Japan; International Institutes for Integrative Sleep Medicine, University of Tsukuba, Ibaraki, Japan.
Toho University · JPTsukuba International University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The demand for meta-analyses in basic biomedical research has been increasing because the phenotyping of genetically modified mice does not always produce consistent results. Melanin-concentrating hormone (MCH) has been reported to be involved in a variety of behaviors that include feeding, body-weight regulation, anxiety, sleep, and reward behavior. However, the reported behavioral and metabolic characteristics of MCH signaling-deficient mice, such as MCH-deficient mice and MCH receptor 1 (MCHR1)-deficient mice, are not consistent with each other. In the present study, we performed a meta-analysis of the published data related to MCH-deficient and MCHR1-deficient mice to obtain robust conclusions about the role of MCH signaling. Overall, the meta-analysis revealed that the deletion of MCH signaling enhanced wakefulness, locomotor activity, aggression, and male sexual behavior and that MCH signaling deficiency suppressed non-REM sleep, anxiety, responses to novelty, startle responses, and conditioned place preferences. In contrast to the acute orexigenic effect of MCH, MCH signaling deficiency significantly increased food intake. Overall, the meta-analysis also revealed that the deletion of MCH signaling suppressed the body weight, fat mass, and plasma leptin, while MCH signaling deficiency increased the body temperature, oxygen consumption, heart rate, and mean arterial pressure. The lean phenotype of the MCH signaling-deficient mice was also confirmed in separate meta-analyses that were specific to sex and background strain (i.e., C57BL/6 and 129Sv). MCH signaling deficiency caused a weak anxiolytic effect as assessed with the elevated plus maze and the open field test but also caused a weak anxiogenic effect as assessed with the emergence test. MCH signaling-deficient mice also exhibited increased plasma corticosterone under non-stressed conditions, which suggests enhanced activity of the hypothalamic-pituitary-adrenal axis. To the best of our knowledge, the present work is the first study to systematically compare the effects of MCH signaling on behavioral and metabolic phenotypes.

Indexed as

Behavior, AnimalAnimalsFemaleHypothalamic HormonesMaleMelaninsMetabolismMiceMice, Inbred C57BLMice, KnockoutPhenotypePituitary HormonesReceptors, SomatostatinSignal TransductionHypothalamic HormonesMchr1 protein, mousemelanin-concentrating hormoneMelaninsPituitary HormonesReceptors, Somatostatin

Identifiers

PMID24924345
PMCPMC4055708
OpenAlexW2030363976

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.