Evidence map›Paper›PMID 12177191›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002

VGF is required for obesity induced by diet, gold thioglucose treatment, and agouti and is differentially regulated in pro-opiomelanocortin- and neuropeptide Y-containing arcuate neurons in response to fasting.

Seung Hahm, Csaba Fekete, Tooru M Mizuno, Joan Windsor, Hai Yan, Carol N Boozer, Charlotte Lee, Joel K Elmquist, Ronald M Lechan, Charles V Mobbs and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

47 citing papers in PubMed, 100 citations in OpenAlex.

  1. Article
  2. Estrogen-Regulated Lateral Septal Kisspeptin Neurons Abundantly Project to GnRH Neurons and the Hypothalamic Supramammillary Nucleus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  3. Structure of AQEE-30 of VGF Neuropeptide in Membrane-Mimicking Environments.International journal of molecular sciences · 2022
    Article
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  17. Neuroendocrine Role for VGF.Frontiers in endocrinology · 2015
    Review
  18. 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

11 authors at 6 institutions in 2 countries.

Seung HahmFishberg Research Center for Neurobiology, Mount Sinai School of Medicine, New York, New York 10029, USA.
Csaba Fekete
Tooru M Mizuno
Joan Windsor
Hai Yan
Carol N Boozer
Charlotte Lee
Joel K Elmquist
Ronald M Lechan
Charles V Mobbs
Stephen R J Salton
Icahn School of Medicine at Mount Sinai · USHarvard University · USAmgen (United States) · USColumbia University · USHUN-REN Institute of Experimental Medicine · HUTufts Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeted deletion of the gene encoding the neuronal and neuroendocrine secreted polypeptide VGF (nonacronymic) produces a lean, hypermetabolic mouse. Consistent with this phenotype, VGF mRNA levels are regulated in the hypothalamic arcuate nucleus in response to fasting. To gain insight into the site(s) and mechanism(s) of action of VGF, we further characterized VGF expression in the hypothalamus. Double-label studies indicated that VGF and pro-opiomelanocortin were coexpressed in lateral arcuate neurons in the fed state, and that VGF expression was induced after fasting in medial arcuate neurons that synthesize neuropeptide Y (NPY). Like NPY, VGF mRNA induction in this region of the hypothalamus in fasted mice was inhibited by exogenous leptin. In leptin-deficient ob/ob and receptor-mutant db/db mice, VGF mRNA levels in the medial arcuate were elevated. To identify neural pathways that are functionally compromised by Vgf ablation, VGF mutant mice were crossed with obese A(y)/a (agouti) and ob/ob mice. VGF deficiency completely blocked the development of obesity in A(y)/a mice, whereas deletion of Vgf in ob/ob mice attenuated weight gain but had no impact on adiposity. Hypothalamic levels of NPY and agouti-related polypeptide mRNAs in both double-mutant lines were dramatically elevated 10- to 15-fold above those of wild-type mice. VGF-deficient mice were also found to resist diet- and gold thioglucose-induced obesity. These data and the susceptibility of VGF mutant mice to monosodium glutamate-induced obesity are consistent with a role for VGF in outflow pathways, downstream of hypothalamic and/or brainstem melanocortin 4 receptors, that project via the autonomic nervous system to peripheral metabolic tissues and regulate energy homeostasis.

Indexed as

DietIntercellular Signaling Peptides and ProteinsAgouti Signaling ProteinAnimalsArcuate Nucleus of HypothalamusAurothioglucoseDisease Models, AnimalEnergy MetabolismFastingGene TargetingImmunohistochemistryIn Situ HybridizationLeptinMaleMiceMice, KnockoutAgouti Signaling ProteinAurothioglucoseIntercellular Signaling Peptides and ProteinsLeptinNerve Growth FactorsNeuropeptidesNeuropeptide YPro-OpiomelanocortinProteinsRNA, MessengerSodium GlutamateVgf protein, mouseVgf protein, rat

Identifiers

PMID12177191
PMCPMC6757869
OpenAlexW1917754098

What Socratic 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 Socratic graph.