Evidence map›Paper›PMID 30842678›Full record

ArticleNature medicine2019

Dysregulation of a long noncoding RNA reduces leptin leading to a leptin-responsive form of obesity.

Olof S Dallner, Jill M Marinis, Yi-Hsueh Lu, Kivanc Birsoy, Emory Werner, Gulya Fayzikhodjaeva, Brian D Dill, Henrik Molina, Arden Moscati, Zoltán Kutalik and 9 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 3% 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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. History and future of leptin: Discovery, regulation and signaling.Metabolism: clinical and experimental · 2024
    Review
  10. Long Noncoding RNAs in Diet-Induced Metabolic Diseases.International journal of molecular sciences · 2024
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Neurolysin Knockout Mice in a Diet-Induced Obesity Model.International journal of molecular sciences · 2023
    Article
  19. Article
  20. Review

9 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 8 institutions in 3 countries.

Olof S DallnerLaboratory of Molecular Genetics, The Rockefeller University, New York, NY, USA.
Jill M MarinisDivision of Endocrinology, Diabetes, and Metabolism and Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA.
Yi-Hsueh LuLaboratory of Molecular Genetics, The Rockefeller University, New York, NY, USA.
Kivanc BirsoyLaboratory of Metabolic Regulation and Genetics, The Rockefeller University, New York, NY, USA.ORCID http://orcid.org/0000-0002-7579-9895
Emory WernerLaboratory of Molecular Genetics, The Rockefeller University, New York, NY, USA.
Gulya FayzikhodjaevaLaboratory of Molecular Genetics, The Rockefeller University, New York, NY, USA.
Brian D DillProteomics Resource Center, The Rockefeller University, New York, NY, USA.ORCID http://orcid.org/0000-0002-4532-3044
Henrik MolinaProteomics Resource Center, The Rockefeller University, New York, NY, USA.
Arden MoscatiThe Charles Bronfman Institute for Personalized Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Zoltán KutalikInstitute of Social and Preventive Medicine, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Pedro Marques-VidalDepartment of Medicine, Internal Medicine, Lausanne University Hospital (CHUV), Lausanne, Switzerland.ORCID http://orcid.org/0000-0002-4548-8500
Tuomas O KilpeläinenNovo Nordisk Foundation Center for Basic Metabolic Research, Section of Metabolic Genetics, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Niels GrarupNovo Nordisk Foundation Center for Basic Metabolic Research, Section of Metabolic Genetics, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.ORCID http://orcid.org/0000-0001-5526-1070
Allan LinnebergCentre for Clinical Research and Prevention, Frederiksberg-Bispebjerg Hospital, Copenhagen, Denmark.ORCID http://orcid.org/0000-0002-0994-0184
Yinxin ZhangLaboratory of Molecular Genetics, The Rockefeller University, New York, NY, USA.ORCID http://orcid.org/0000-0001-5909-3676
Roger VaughanDepartment of Biostatistics, The Rockefeller University, New York, NY, USA.
Ruth J F LoosThe Charles Bronfman Institute for Personalized Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Mitchell A LazarDivision of Endocrinology, Diabetes, and Metabolism and Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA.
Jeffrey M FriedmanLaboratory of Molecular Genetics, The Rockefeller University, New York, NY, USA. friedj@rockefeller.edu.ORCID http://orcid.org/0000-0003-2152-0868
Rockefeller University · USUniversity of Copenhagen · DKUniversity of Pennsylvania · USChild Health and Development Institute · USHoward Hughes Medical Institute · USIcahn School of Medicine at Mount Sinai · USSIB Swiss Institute of Bioinformatics · CHUniversity of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Quantitative changes in leptin concentration lead to alterations in food intake and body weight, but the regulatory mechanisms that control leptin gene expression are poorly understood. Here we report that fat-specific and quantitative leptin expression is controlled by redundant cis elements and trans factors interacting with the proximal promoter together with a long noncoding RNA (lncOb). Diet-induced obese mice lacking lncOb show increased fat mass with reduced plasma leptin levels and lose weight after leptin treatment, whereas control mice do not. Consistent with this finding, large-scale genetic studies of humans reveal a significant association of single-nucleotide polymorphisms (SNPs) in the region of human lncOb with lower plasma leptin levels and obesity. These results show that reduced leptin gene expression can lead to a hypoleptinemic, leptin-responsive form of obesity and provide a framework for elucidating the pathogenic mechanism in the subset of obese patients with low endogenous leptin levels.

Indexed as

AnimalsBody WeightDiet, High-FatEatingEnhancer Elements, GeneticFemaleGene Expression RegulationHumansLeptinMaleMiceMice, KnockoutMice, TransgenicObesityPolymorphism, Single NucleotideRNA, Long NoncodingLeptinRNA, Long Noncoding

Identifiers

PMID30842678
OpenAlexW2918488914

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.