Evidence map›Paper›PMID 29174000›Full record

ArticleMolecular metabolism2018

Deficiency of leptin receptor in myeloid cells disrupts hypothalamic metabolic circuits and causes body weight increase.

Yuanqing Gao, Andrés Vidal-Itriago, Irina Milanova, Nikita L Korpel, Martin J Kalsbeek, Robby Zachariah Tom, Andries Kalsbeek, Susanna M Hofmann, Chun-Xia Yi

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

34 citing papers in PubMed, 61 citations in OpenAlex.

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  6. Microglia in Central Control of Metabolism.Physiology (Bethesda, Md.) · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

Yuanqing GaoDepartment of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, The Netherlands.
Andrés Vidal-ItriagoDepartment of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, The Netherlands.
Irina MilanovaDepartment of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, The Netherlands.
Nikita L KorpelDepartment of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, The Netherlands.
Martin J KalsbeekDepartment of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, The Netherlands.
Robby Zachariah TomInstitute for Diabetes and Regeneration Research & Helmholtz Diabetes Center, Helmholtz Zentrum München, Germany.
Andries KalsbeekDepartment of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, The Netherlands; Hypothalamic Integration Mechanisms, Netherlands Institute for Neuroscience, Amsterdam, The Netherlands.
Susanna M HofmannInstitute for Diabetes and Regeneration Research & Helmholtz Diabetes Center, Helmholtz Zentrum München, Germany; German Center for Diabetes Research (DZD), Neuherberg, Germany; Medizinische Klinik und Poliklinik IV, Klinikum der LMU, München, Germany.
Chun-Xia YiDepartment of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, The Netherlands. Electronic address: c.yi@amc.uva.nl.
Amsterdam UMC Location University of Amsterdam · NLUniversity of Amsterdam · NLHeinrich Heine University Düsseldorf · DEHelmholtz Zentrum München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveLeptin is a cytokine produced by adipose tissue that acts mainly on the hypothalamus to regulate appetite and energy homeostasis. Previous studies revealed that the leptin receptor is expressed not only in neurons, but also in glial cells. Microglia are resident immune cells in the brain that play an essential role in immune defense and neural network development. Previously we reported that microglial morphology and cytokine production are changed in the leptin receptor deficient db/db mouse, suggesting that leptin's central effects on metabolic control might involve signaling through microglia. In the current study, we aimed to uncover the role of leptin signaling in microglia in systemic metabolic control.

methodsWe generated a mouse model with leptin receptor deficiency, specifically in the myeloid cells, to determine the role of microglial leptin signaling in the development of metabolic disease and to investigate microglial functions.

resultsWe discovered that these mice have increased body weight with hyperphagia. In the hypothalamus, pro-opiomelanocortin neuron numbers in the arcuate nucleus (ARC) and α-MSH projections from the ARC to the paraventricular nucleus (PVN) decreased, which was accompanied by the presence of less ramified microglia with impaired phagocytic capacity in the PVN.

conclusionsMyeloid cell leptin receptor deficient mice partially replicate the db/db phenotype. Leptin signaling in hypothalamic microglia is important for microglial function and a correct formation of the hypothalamic neuronal circuit regulating metabolism.

Indexed as

Weight GainAnimalsArcuate Nucleus of HypothalamusCells, CulturedHyperphagiaMiceMicrogliaMyeloid CellsParaventricular Hypothalamic NucleusPhagocytosisReceptors, LeptinReceptors, LeptinDiabetesMicrogliaObesityPOMCα-MSH

Identifiers

PMID29174000
PMCPMC5784319
OpenAlexW2767862238

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.