Evidence map›Paper›PMID 22285542›Full record

ArticleCell metabolism2012

Loss of autophagy in pro-opiomelanocortin neurons perturbs axon growth and causes metabolic dysregulation.

Bérengère Coupé, Yuko Ishii, Marcelo O Dietrich, Masaaki Komatsu, Tamas L Horvath, Sebastien G Bouret

Open access · bronzeAbstract read
In one paragraph

Article in Cell metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 1 pooled it
6.6field-weighted citation impact, top 2% 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

102 citing papers in PubMed, 1 synthesis or guideline pooled it, 169 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Hypothalamic regulation of energy homeostasis: Quo vadis.Reviews in endocrine & metabolic disorders · 2026
    Review
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  20. Leptin signaling and leptin resistance.Medical review (2021) · 2022
    Review

42 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

6 authors at 4 institutions in 4 countries.

Bérengère CoupéThe Saban Research Institute, Neuroscience Program, Children's Hospital Los Angeles, University of Southern California, Los Angeles, CA 90027, USA.
Yuko Ishii
Marcelo O Dietrich
Masaaki Komatsu
Tamas L Horvath
Sebastien G Bouret
Children's Hospital of Los Angeles · USYale University · USJuntendo University · JPUniversity of Southern California · US

Funding

Leptin and the Nutritional Programming of Obesity and DiabetesR01DK084142 · NIDDK · CHILDREN'S HOSPITAL OF LOS ANGELES · PI LEVITT, PAT · 2010 to 2022
$4.3M
Hypothalamic AgRP Neurons Are Determinants of Healthy Lifespan and Higher Brain DP1DK098058 · NIDDK · YALE UNIVERSITY · PI HORVATH, TAMAS L · 2012 to 2014
$2.4M
Developmental insulin/leptin signaling determines set-point of the adult melanocoR01DK080000 · NIDDK · YALE UNIVERSITY · PI HORVATH, TAMAS L · 2008 to 2011
$1.5M
NIDDK NIH HHS DK080000NIDDK NIH HHS DK84142NIDDK NIH HHS DP1 DK098058NIDDK NIH HHS R01 DK080000NIDDK NIH HHS R01 DK084142
6 · The paper itself

Abstract

The hypothalamic melanocortin system, which includes neurons that produce pro-opiomelanocortin (POMC)-derived peptides, is a major negative regulator of energy balance. POMC neurons begin to acquire their unique properties during neonatal life. The formation of functional neural systems requires massive cytoplasmic remodeling that may involve autophagy, an important intracellular mechanism for the degradation of damaged proteins and organelles. Here we investigated the functional and structural effects of the deletion of an essential autophagy gene, Atg7, in POMC neurons. Lack of Atg7 in POMC neurons caused higher postweaning body weight, increased adiposity, and glucose intolerance. These metabolic impairments were associated with an age-dependent accumulation of ubiquitin/p62-positive aggregates in the hypothalamus and a disruption in the maturation of POMC-containing axonal projections. Together, these data provide direct genetic evidence that Atg7 in POMC neurons is required for normal metabolic regulation and neural development, and they implicate hypothalamic autophagy deficiency in the pathogenesis of obesity.

Indexed as

AdiposityAnimalsArcuate Nucleus of HypothalamusAutophagyAutophagy-Related Protein 7AxonsBody WeightGlucose IntoleranceImmunoblottingMetabolic Networks and PathwaysMiceMicroscopy, ElectronMicrotubule-Associated ProteinsNeuronsPro-OpiomelanocortinTranscription FactorsAtg7 protein, mouseAutophagy-Related Protein 7Gtf2h1 protein, mouseMicrotubule-Associated ProteinsPro-OpiomelanocortinTranscription FactorsTranscription Factor TFIIHUbiquitin

Identifiers

PMID22285542
PMCPMC3278575
OpenAlexW1990413385

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.