Evidence map›Paper›PMID 34448070›Full record

ReviewMolecular and cellular pediatrics2021

A fresh look to the phenotype in mono-allelic likely pathogenic variants of the leptin and the leptin receptor gene.

Ingrid Koerber-Rosso, Stephanie Brandt, Julia von Schnurbein, Pamela Fischer-Posovszky, Josef Hoegel, Hannah Rabenstein, Reiner Siebert, Martin Wabitsch

Open access · goldAbstract readReview
In one paragraph

Review in Molecular and cellular pediatrics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
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  6. Viruses · 2022
    Article
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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

8 authors at 1 institution in 1 country.

Ingrid Koerber-Rosso *Division of Pediatric Endocrinology and Diabetes, Department of Pediatrics and Adolescent Medicine, University Medical Center Ulm, Ulm, Germany.
Stephanie Brandt *Division of Pediatric Endocrinology and Diabetes, Department of Pediatrics and Adolescent Medicine, University Medical Center Ulm, Ulm, Germany.ORCID http://orcid.org/0000-0002-8693-2647
Julia von SchnurbeinDivision of Pediatric Endocrinology and Diabetes, Department of Pediatrics and Adolescent Medicine, University Medical Center Ulm, Ulm, Germany.
Pamela Fischer-PosovszkyDivision of Pediatric Endocrinology and Diabetes, Department of Pediatrics and Adolescent Medicine, University Medical Center Ulm, Ulm, Germany.
Josef HoegelInstitute of Human Genetics, University of Ulm, University Medical Center Ulm, Ulm, Germany.
Hannah RabensteinInstitute of Human Genetics, University of Ulm, University Medical Center Ulm, Ulm, Germany.
Reiner SiebertInstitute of Human Genetics, University of Ulm, University Medical Center Ulm, Ulm, Germany.
Martin WabitschDivision of Pediatric Endocrinology and Diabetes, Department of Pediatrics and Adolescent Medicine, University Medical Center Ulm, Ulm, Germany. martin.wabitsch@uniklinik-ulm.de.
Universität Ulm · DE

Funding

Competence Network Obesity FKZ 01GI1401German Ministry of Education and Research (BMBF) FKZ 01GI1120A and 01GI1127German Research Association FI1700/7-1, Heisenberg ProfessorshipHertha-Nathorff-Programm of the Medical Faculty of the University of Ulm KSKI, 002.1Hertha-Nathorff-Programm of the Medical Faculty of the University of Ulm LSSH1000.07
6 · The paper itself

Abstract

Leptin (LEP) and leptin receptor (LEPR) play a major role in energy homeostasis, metabolism, and reproductive function. While effects of biallelic likely pathogenic variants (-/-) on the phenotype are well characterized, effects of mono-allelic likely pathogenic variants (wt/-) in the LEP and LEPR gene on the phenotype compared to wild-type homozygosity (wt/wt) have not been systematically investigated. We identified in our systematic review 44 animal studies (15 on Lep, 29 on Lepr) and 39 studies in humans reporting on 130 mono-allelic likely pathogenic variant carriers with 20 distinct LEP variants and 108 heterozygous mono-allelic likely pathogenic variant carriers with 35 distinct LEPR variants. We found indications for a higher weight status in carriers of mono-allelic likely pathogenic variant in the leptin and in the leptin receptor gene compared to wt/wt, in both animal and human studies. In addition, animal studies showed higher body fat percentage in Lep and Lepr wt/- vs wt/wt. Animal studies provided indications for lower leptin levels in Lep wt/- vs. wt/wt and indications for higher leptin levels in Lepr wt/- vs wt/wt. Data on leptin levels in human studies was limited. Evidence for an impaired metabolism in mono-allelic likely pathogenic variants of the leptin and in leptin receptor gene was not conclusive (animal and human studies). Mono-allelic likely pathogenic variants in the leptin and in leptin receptor gene have phenotypic effects disposing to increased body weight and fat accumulation.

Indexed as

AnimalHumansLEPLEPRPhenotype

Identifiers

PMID34448070
PMCPMC8390564
OpenAlexW3195561835

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.