Evidence map›Paper›PMID 25016380›Full record

ArticleJournal of lipid research2014

Inhibition of the central melanocortin system decreases brown adipose tissue activity.

Sander Kooijman, Mariëtte R Boon, Edwin T Parlevliet, Janine J Geerling, Vera van de Pol, Johannes A Romijn, Louis M Havekes, Illiana Meurs, Patrick C N Rensen

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

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  12. [Scientific reports · 2019
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  14. Neonatal tobacco smoke reduces thermogenesis capacity in brown adipose tissue in adult rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018
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  19. Prolonged daily light exposure increases body fat mass through attenuation of brown adipose tissue activity.Proceedings of the National Academy of Sciences of the United States of America · 2015
    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

9 authors at 3 institutions in 1 country.

Sander KooijmanDepartment of Endocrinology and Metabolic Diseases, Leiden University Medical Center, Leiden, The Netherlands Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands.
Mariëtte R BoonDepartment of Endocrinology and Metabolic Diseases, Leiden University Medical Center, Leiden, The Netherlands Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands.
Edwin T ParlevlietDepartment of Endocrinology and Metabolic Diseases, Leiden University Medical Center, Leiden, The Netherlands Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands Department of Internal Medicine, Academic Medical Center, University of Amsterdam, The Netherlands.
Janine J GeerlingDepartment of Endocrinology and Metabolic Diseases, Leiden University Medical Center, Leiden, The Netherlands Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands.
Vera van de PolDepartment of Endocrinology and Metabolic Diseases, Leiden University Medical Center, Leiden, The Netherlands Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands.
Johannes A RomijnDepartment of Internal Medicine, Academic Medical Center, University of Amsterdam, The Netherlands.
Louis M HavekesDepartment of Endocrinology and Metabolic Diseases, Leiden University Medical Center, Leiden, The Netherlands Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands Netherlands Organization for Applied Scientific Research, Gaubius Laboratory, Leiden, The Netherlands.
Illiana MeursDepartment of Endocrinology and Metabolic Diseases, Leiden University Medical Center, Leiden, The Netherlands Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands.
Patrick C N RensenDepartment of Endocrinology and Metabolic Diseases, Leiden University Medical Center, Leiden, The Netherlands Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands.
Leiden University Medical Center · NLUniversity of Amsterdam · NLNetherlands Organisation for Applied Scientific Research · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The melanocortin system is an important regulator of energy balance, and melanocortin 4 receptor (MC4R) deficiency is the most common monogenic cause of obesity. We investigated whether the relationship between melanocortin system activity and energy expenditure (EE) is mediated by brown adipose tissue (BAT) activity. Therefore, female APOE*3-Leiden.CETP transgenic mice were fed a Western-type diet for 4 weeks and infused intracerebroventricularly with the melanocortin 3/4 receptor (MC3/4R) antagonist SHU9119 or vehicle for 2 weeks. SHU9119 increased food intake (+30%) and body fat (+50%) and decreased EE by reduction in fat oxidation (-42%). In addition, SHU9119 impaired the uptake of VLDL-TG by BAT. In line with this, SHU9119 decreased uncoupling protein-1 levels in BAT (-60%) and induced large intracellular lipid droplets, indicative of severely disturbed BAT activity. Finally, SHU9119-treated mice pair-fed to the vehicle-treated group still exhibited these effects, indicating that MC4R inhibition impairs BAT activity independent of food intake. These effects were not specific to the APOE*3-Leiden.CETP background as SHU9119 also inhibited BAT activity in wild-type mice. We conclude that inhibition of central MC3/4R signaling impairs BAT function, which is accompanied by reduced EE, thereby promoting adiposity. We anticipate that activation of MC4R is a promising strategy to combat obesity by increasing BAT activity.

Indexed as

Adipose Tissue, BrownAnimalsApolipoprotein E3FemaleMelanocyte-Stimulating HormonesMiceMice, TransgenicOxidation-ReductionReceptor, Melanocortin, Type 3Receptor, Melanocortin, Type 4Signal TransductionApolipoprotein E3Mc3r protein, mouseMC4R protein, mouseMelanocyte-Stimulating HormonesReceptor, Melanocortin, Type 3Receptor, Melanocortin, Type 4SHU 9119energy expenditurelivertriglyceridesvery low density lipoproteinwhite adipose tissue

Identifiers

PMID25016380
PMCPMC4173995
OpenAlexW2154639886

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.