Evidence map›Paper›PMID 24462248›Full record

ArticleCell2014

Neonatal insulin action impairs hypothalamic neurocircuit formation in response to maternal high-fat feeding.

Merly C Vogt, Lars Paeger, Simon Hess, Sophie M Steculorum, Motoharu Awazawa, Brigitte Hampel, Susanne Neupert, Hayley T Nicholls, Jan Mauer, A Christine Hausen and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 192 papers.

0numbers the graph read from it
0cells of the map it votes in
192citing papers in PubMed
15.9field-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

192 citing papers in PubMed, 355 citations in OpenAlex.

  1. Article
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  5. Tanycytes: bloodhounds of the metabolic brain.Trends in endocrinology and metabolism: TEM · 2026
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  11. Heart Rate Variability in Newborns From Diabetic Mothers: Clinical Application and Significance.Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc · 2026
    Review
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132 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 2 countries.

Merly C VogtMax Planck Institute for Neurological Research, 50931 Cologne, Germany; Department of Mouse Genetics and Metabolism, Institute for Genetics, University of Cologne, 50674 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, 50674 Cologne, Germany.
Lars PaegerBiocenter, Institute for Zoology, University of Cologne, 50674 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, 50674 Cologne, Germany.
Simon HessBiocenter, Institute for Zoology, University of Cologne, 50674 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, 50674 Cologne, Germany.
Sophie M SteculorumMax Planck Institute for Neurological Research, 50931 Cologne, Germany; Department of Mouse Genetics and Metabolism, Institute for Genetics, University of Cologne, 50674 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, 50674 Cologne, Germany.
Motoharu AwazawaMax Planck Institute for Neurological Research, 50931 Cologne, Germany; Department of Mouse Genetics and Metabolism, Institute for Genetics, University of Cologne, 50674 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, 50674 Cologne, Germany.
Brigitte HampelMax Planck Institute for Neurological Research, 50931 Cologne, Germany; Department of Mouse Genetics and Metabolism, Institute for Genetics, University of Cologne, 50674 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, 50674 Cologne, Germany.
Susanne NeupertBiocenter, Institute for Zoology, University of Cologne, 50674 Cologne, Germany.
Hayley T NichollsMax Planck Institute for Neurological Research, 50931 Cologne, Germany; Department of Mouse Genetics and Metabolism, Institute for Genetics, University of Cologne, 50674 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, 50674 Cologne, Germany.
Jan MauerMax Planck Institute for Neurological Research, 50931 Cologne, Germany; Department of Mouse Genetics and Metabolism, Institute for Genetics, University of Cologne, 50674 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, 50674 Cologne, Germany.
A Christine HausenMax Planck Institute for Neurological Research, 50931 Cologne, Germany; Department of Mouse Genetics and Metabolism, Institute for Genetics, University of Cologne, 50674 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, 50674 Cologne, Germany.
Reinhard PredelBiocenter, Institute for Zoology, University of Cologne, 50674 Cologne, Germany.
Peter KloppenburgBiocenter, Institute for Zoology, University of Cologne, 50674 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, 50674 Cologne, Germany.
Tamas L HorvathProgram in Integrative Cell Signaling and Neurobiology of Metabolism, Section of Comparative Medicine, Department of Obstetrics/Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT 06510, USA. Electronic address: tamas.horvath@yale.edu.
Jens C BrüningMax Planck Institute for Neurological Research, 50931 Cologne, Germany; Department of Mouse Genetics and Metabolism, Institute for Genetics, University of Cologne, 50674 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), University of Cologne, 50674 Cologne, Germany; Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, 50924 Cologne, Germany. Electronic address: bruening@nf.mpg.de.
Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEUniversity of Cologne · DEMax Planck Institute for Metabolism Research · DEYale University · US

Funding

Hypothalamic AgRP Neurons Are Determinants of Healthy Lifespan and Higher Brain DP1DK098058 · NIDDK · YALE UNIVERSITY · PI HORVATH, TAMAS L · 2012 to 2014
$2.4M
NIDDK NIH HHS DP1 DK098058
6 · The paper itself

Abstract

Maternal metabolic homeostasis exerts long-term effects on the offspring's health outcomes. Here, we demonstrate that maternal high-fat diet (HFD) feeding during lactation predisposes the offspring for obesity and impaired glucose homeostasis in mice, which is associated with an impairment of the hypothalamic melanocortin circuitry. Whereas the number and neuropeptide expression of anorexigenic proopiomelanocortin (POMC) and orexigenic agouti-related peptide (AgRP) neurons, electrophysiological properties of POMC neurons, and posttranslational processing of POMC remain unaffected in response to maternal HFD feeding during lactation, the formation of POMC and AgRP projections to hypothalamic target sites is severely impaired. Abrogating insulin action in POMC neurons of the offspring prevents altered POMC projections to the preautonomic paraventricular nucleus of the hypothalamus (PVH), pancreatic parasympathetic innervation, and impaired glucose-stimulated insulin secretion in response to maternal overnutrition. These experiments reveal a critical timing, when altered maternal metabolism disrupts metabolic homeostasis in the offspring via impairing neuronal projections, and show that abnormal insulin signaling contributes to this effect.

Indexed as

Diet, High-FatLactationAnimalsAxonsFemaleHyperglycemiaHypothalamusInsulinMaleMetabolic DiseasesMiceMice, Inbred C57BLNeuronsObesityPregnancyPro-OpiomelanocortinInsulinPro-OpiomelanocortinReceptor, Insulin

Identifiers

PMID24462248
PMCPMC4101521
OpenAlexW1987922392

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.