Evidence map›Paper›PMID 29742429›Full record

ArticleCell reports2018

Diet-Induced Growth Is Regulated via Acquired Leptin Resistance and Engages a Pomc-Somatostatin-Growth Hormone Circuit.

Heiko Löhr, Simon Hess, Mafalda M A Pereira, Philip Reinoß, Sandra Leibold, Christel Schenkel, Claudia M Wunderlich, Peter Kloppenburg, Jens C Brüning, Matthias Hammerschmidt

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 51 citations in OpenAlex.

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  8. Leptin treatment has vasculo-protective effects in lipodystrophic mice.Proceedings of the National Academy of Sciences of the United States of America · 2022
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  15. Pomc Plays an Important Role in Sexual Size Dimorphism in Tilapia.Marine biotechnology (New York, N.Y.) · 2021
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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

10 authors at 3 institutions in 1 country.

Heiko LöhrInstitute of Zoology, University of Cologne, Cologne, Germany.
Simon HessInstitute of Zoology, University of Cologne, Cologne, Germany.
Mafalda M A PereiraDepartment of Neuronal Control of Metabolism, Max Planck Institute for Metabolism Research, Cologne, Germany.
Philip ReinoßInstitute of Zoology, University of Cologne, Cologne, Germany.
Sandra LeiboldInstitute of Zoology, University of Cologne, Cologne, Germany.
Christel SchenkelInstitute of Zoology, University of Cologne, Cologne, Germany.
Claudia M WunderlichDepartment of Neuronal Control of Metabolism, Max Planck Institute for Metabolism Research, Cologne, Germany.
Peter KloppenburgInstitute of Zoology, University of Cologne, Cologne, Germany; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, Cologne, Germany.
Jens C BrüningDepartment of Neuronal Control of Metabolism, Max Planck Institute for Metabolism Research, Cologne, Germany; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, Cologne, Germany; Center for Molecular Medicine Cologne, University of Cologne, Cologne, Germany.
Matthias HammerschmidtInstitute of Zoology, University of Cologne, Cologne, Germany; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, Cologne, Germany; Center for Molecular Medicine Cologne, University of Cologne, Cologne, Germany. Electronic address: mhammers@uni-koeln.de.
University of Cologne · DEMax Planck Institute for Metabolism Research · DECologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DE

Funding

Systematic Vertebrate Functional GenomicsR01GM063904 · NIGMS · UNIVERSITY OF TEXAS AT AUSTIN · PI EKKER, STEPHEN CARL · 2001 to 2025
$10.7M
Systematic Vertebrate Functional GenomicsR56GM063904 · NIGMS · MAYO CLINIC ROCHESTER · PI EKKER, STEPHEN CARL · 2009 to 2010
$611k
NIGMS NIH HHS R01 GM063904NIGMS NIH HHS R56 GM063904
6 · The paper itself

Abstract

Anorexigenic pro-opiomelanocortin (Pomc)/alpha-melanocyte stimulating hormone (αMSH) neurons of the hypothalamic melanocortin system function as key regulators of energy homeostasis, also controlling somatic growth across different species. However, the mechanisms of melanocortin-dependent growth control still remain ill-defined. Here, we reveal a thus-far-unrecognized structural and functional connection between Pomc neurons and the somatotropic hypothalamo-pituitary axis. Excessive feeding of larval zebrafish causes leptin resistance and reduced levels of the hypothalamic satiety mediator pomca. In turn, this leads to reduced activation of hypophysiotropic somatostatin (Sst)-neurons that express the melanocortin receptor Mc4r, elevated growth hormone (GH) expression in the pituitary, and enhanced somatic growth. Mc4r expression and αMSH responsiveness are conserved in Sst-expressing hypothalamic neurons of mice. Thus, acquired leptin resistance and attenuation of pomca transcription in response to excessive caloric intake may represent an ancient mechanism to promote somatic growth when food resources are plentiful.

Indexed as

Dietalpha-MSHAnimalsAxonsGrowth and DevelopmentGrowth HormoneHumansHypothalamusLarvaLeptinLipid MetabolismMice, Inbred C57BLMice, TransgenicNeural InhibitionPituitary Gland, AnteriorPro-Opiomelanocortinalpha-MSHGrowth HormoneLeptinPro-OpiomelanocortinSomatostatingrowth hormonehigh-fat dietleptin resistancemelanocortin systemmouseobesityPomc neuronsomatic growthsomatostatin neuronzebrafish

Identifiers

PMID29742429
PMCPMC6015746
OpenAlexW2801224022

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.