Evidence map›Paper›PMID 27106110›Full record

ArticleThe Journal of endocrinology2016

Loss of Mrap2 is associated with Sim1 deficiency and increased circulating cholesterol.

T V Novoselova, R Larder, D Rimmington, C Lelliott, E H Wynn, R J Gorrigan, P H Tate, L Guasti, Sanger Mouse Genetics Project, S O'Rahilly and 4 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 2 pooled it
2.8field-weighted citation impact, top 10% 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, 2 syntheses or guidelines pooled it, 46 citations in OpenAlex.

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  18. The central melanocortin system and human obesity.Journal of molecular cell biology · 2020
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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

14 authors at 5 institutions in 1 country.

T V NovoselovaCentre for EndocrinologyQueen Mary University of London, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London, UK.
R LarderUniversity of Cambridge Metabolic Research LaboratoriesMRC Metabolic Disease Unit, Wellcome Trust-MRC Institute of Metabolic Science and NIHR Cambridge Biomedical Research Centre, Addenbrooke's Hospital, Cambridge, UK.
D RimmingtonUniversity of Cambridge Metabolic Research LaboratoriesMRC Metabolic Disease Unit, Wellcome Trust-MRC Institute of Metabolic Science and NIHR Cambridge Biomedical Research Centre, Addenbrooke's Hospital, Cambridge, UK.
C LelliottWellcome Trust Sanger InstituteWellcome Trust Genome Campus, Hinxton, Cambridge, UK.
E H WynnWellcome Trust Sanger InstituteWellcome Trust Genome Campus, Hinxton, Cambridge, UK.
R J GorriganCentre for EndocrinologyQueen Mary University of London, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London, UK.
P H TateWellcome Trust Sanger InstituteWellcome Trust Genome Campus, Hinxton, Cambridge, UK.
L GuastiCentre for EndocrinologyQueen Mary University of London, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London, UK.
Sanger Mouse Genetics Project
S O'RahillyUniversity of Cambridge Metabolic Research LaboratoriesMRC Metabolic Disease Unit, Wellcome Trust-MRC Institute of Metabolic Science and NIHR Cambridge Biomedical Research Centre, Addenbrooke's Hospital, Cambridge, UK.
A J L ClarkCentre for EndocrinologyQueen Mary University of London, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London, UK a.j.clark@qmul.ac.uk.
D W LoganWellcome Trust Sanger InstituteWellcome Trust Genome Campus, Hinxton, Cambridge, UK.
A P CollUniversity of Cambridge Metabolic Research LaboratoriesMRC Metabolic Disease Unit, Wellcome Trust-MRC Institute of Metabolic Science and NIHR Cambridge Biomedical Research Centre, Addenbrooke's Hospital, Cambridge, UK.
L F ChanCentre for EndocrinologyQueen Mary University of London, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London, UK.
Wellcome Sanger Institute · GBWilliam Harvey Research Institute · GBAddenbrooke's Hospital · GBQueen Mary University of London · GBUniversity of Cambridge · GB

Funding

Biotechnology and Biological Sciences Research Council BB/L00267/1Medical Research Council G0802796Medical Research Council MC_UU_12012/1Medical Research Council MC_UU_12012/5Wellcome Trust 098051Wellcome Trust WBIB92024MA
6 · The paper itself

Abstract

Melanocortin receptor accessory protein 2 (MRAP2) is a transmembrane accessory protein predominantly expressed in the brain. Both global and brain-specific deletion of Mrap2 in mice results in severe obesity. Loss-of-function MRAP2 mutations have also been associated with obesity in humans. Although MRAP2 has been shown to interact with MC4R, a G protein-coupled receptor with an established role in energy homeostasis, appetite regulation and lipid metabolism, the mechanisms through which loss of MRAP2 causes obesity remains uncertain. In this study, we used two independently derived lines of Mrap2 deficient mice (Mrap2(tm1a/tm1a)) to further study the role of Mrap2 in the regulation of energy balance and peripheral lipid metabolism. Mrap2(tm1a/tm1a) mice have a significant increase in body weight, with increased fat and lean mass, but without detectable changes in food intake or energy expenditure. Transcriptomic analysis showed significantly decreased expression of Sim1, Trh, Oxt and Crh within the hypothalamic paraventricular nucleus of Mrap2(tm1a/tm1a) mice. Circulating levels of both high-density lipoprotein and low-density lipoprotein were significantly increased in Mrap2 deficient mice. Taken together, these data corroborate the role of MRAP2 in metabolic regulation and indicate that, at least in part, this may be due to defective central melanocortin signalling.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAnxietyBasic Helix-Loop-Helix ProteinsBehavior, AnimalBody WeightCholesterolCorticotropin-Releasing HormoneEatingEnergy MetabolismLipid MetabolismMiceMice, KnockoutMotor ActivityNeuronsOxytocinAdaptor Proteins, Signal TransducingBasic Helix-Loop-Helix ProteinsCholesterolCorticotropin-Releasing HormoneMRAP2 protein, mouseOxytocinReceptor Activity-Modifying ProteinsRepressor ProteinsSim1 protein, mouseThyrotropin-Releasing Hormoneaccessory proteinAVPCRHMC4RmelanocortinmetabolismMRAP2obesityOXTSIM1TRH

Identifiers

PMID27106110
PMCPMC5064762
OpenAlexW2340823654

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.