Evidence map›Paper›PMID 25232147›Full record

ReviewThe Journal of endocrinology2014

20 years of leptin: connecting leptin signaling to biological function.

Margaret B Allison, Martin G Myers

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed, 2 pooled it
9.6field-weighted citation impact, top 1% 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

114 citing papers in PubMed, 2 syntheses or guidelines pooled it, 223 citations in OpenAlex.

  1. Classification of Congenital Leptin Deficiency.The Journal of clinical endocrinology and metabolism · 2024
    Pooled it
  2. Pooled it
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  11. Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025
    Review
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54 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Margaret B AllisonDepartments of Internal Medicineand Molecular and Integrative Physiology, University of Michigan, 1000 Wall Street, 6317 Brehm Tower, Ann Arbor, Michigan 48105, USA.
Martin G MyersDepartments of Internal Medicineand Molecular and Integrative Physiology, University of Michigan, 1000 Wall Street, 6317 Brehm Tower, Ann Arbor, Michigan 48105, USA mgmyers@umich.edu.
University of Michigan–Ann Arbor · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Scott Soleimanpour · 2013 to 2026
$24.3M
MOLECULAR DETERMINANTS OF LEPTIN RECEPTOR/JAK2 SIGNALINGR01DK056731 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MYERS, MARTIN G · 1999 to 2025
$6.0M
Molecular Mechanisms of Leptin Receptor/Jak2 ActionR37DK056731 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MYERS, MARTIN G · 2008 to 2017
$3.5M
Role of the Lateral Hypothalamic Area in Leptin ActionR01DK078056 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MYERS, MARTIN G · 2008 to 2017
$3.4M
A Leptin-Regulated Brainstem Pathway That Controls Glucose and Energy HomeostasisR01DK098853 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MYERS, MARTIN G · 2014 to 2017
$1.4M
Role of DMH LepR-b neurons in leptin actionF30DK097861 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ALLISON, MARGARET B · 2012 to 2014
$104k
NIDDK NIH HHS DK056731NIDDK NIH HHS DK097861NIDDK NIH HHS DK098853NIDDK NIH HHS DK78056NIDDK NIH HHS F30 DK097861NIDDK NIH HHS P30 DK020572NIDDK NIH HHS R01 DK056731NIDDK NIH HHS R01 DK078056NIDDK NIH HHS R01 DK098853NIDDK NIH HHS R37 DK056731
6 · The paper itself

Abstract

Hypothalamic leptin action promotes negative energy balance and modulates glucose homeostasis, as well as serving as a permissive signal to the neuroendocrine axes that control growth and reproduction. Since the initial discovery of leptin 20 years ago, we have learned a great deal about the molecular mechanisms of leptin action. An important aspect of this has been the dissection of the cellular mechanisms of leptin signaling, and how specific leptin signals influence physiology. Leptin acts via the long form of the leptin receptor LepRb. LepRb activation and subsequent tyrosine phosphorylation recruits and activates multiple signaling pathways, including STAT transcription factors, SHP2 and ERK signaling, the IRS-protein/PI3Kinase pathway, and SH2B1. Each of these pathways controls specific aspects of leptin action and physiology. Important inhibitory pathways mediated by suppressor of cytokine signaling proteins and protein tyrosine phosphatases also limit physiologic leptin action. This review summarizes the signaling pathways engaged by LepRb and their effects on energy balance, glucose homeostasis, and reproduction. Particular emphasis is given to the multiple mouse models that have been used to elucidate these functions in vivo.

Indexed as

AnimalsBrainEnergy MetabolismGlucoseHomeostasisHumansLeptinReceptors, LeptinReproductionSignal TransductionGlucoseLeptinReceptors, Leptinhypothalamusleptinobesitysignal transduction

Identifiers

PMID25232147
PMCPMC4170570
OpenAlexW2101667330

What OpenQuestion holds

Textmetadata
LicenceTDM
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.