Evidence map›Paper›PMID 23640886›Full record

ArticleThe Journal of biological chemistry2013

Obesity induces hypothalamic endoplasmic reticulum stress and impairs proopiomelanocortin (POMC) post-translational processing.

Isin Cakir, Nicole E Cyr, Mario Perello, Bogdan Patedakis Litvinov, Amparo Romero, Ronald C Stuart, Eduardo A Nillni

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 104 citations in OpenAlex.

  1. Hypothalamic endoplasmic reticulum stress drives pubertal precocity due to early-onset obesity in female rodents.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Review
  3. Medium-Chain Fatty Acids Extracted from Black Soldier Fly (Animals : an open access journal from MDPI · 2025
    Article
  4. Article
  5. Crosstalk between MSC-extracellular vesicles andFrontiers in pharmacology · 2025
    Article
  6. Review
  7. Obesity Alters POMC and Kisspeptin Neuron Cross Talk Leading to Reduced Luteinizing Hormone in Male Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  8. The Mechanism of Leptin Resistance in Obesity and Therapeutic Perspective.Advances in experimental medicine and biology · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Leptin as a key regulator of the adipose organ.Reviews in endocrine & metabolic disorders · 2022
    Review
  13. Review
  14. UPRFrontiers in cell and developmental biology · 2022
    Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Hypothalamic extended synaptotagmin-3 contributes to the development of dietary obesity and related metabolic disorders.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
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

7 authors at 2 institutions in 1 country.

Isin CakirDivision of Endocrinology, Department of Medicine, Warren Alpert Medical School of Brown University/Rhode Island Hospital, Providence, Rhode Island 02907, USA.
Nicole E Cyr
Mario Perello
Bogdan Patedakis Litvinov
Amparo Romero
Ronald C Stuart
Eduardo A Nillni
Brown University · USRhode Island Hospital · US

Funding

Hypothalamic SIRT1 and Energy BalanceR01DK085916 · NIDDK · RHODE ISLAND HOSPITAL · PI NILLNI, EDUARDO A. · 2010 to 2013
$1.4M
NIDDK NIH HHS R01 DK085916NIDDK NIH HHS R01 DK085916-01
6 · The paper itself

Abstract

It was shown previously that abnormal prohormone processing or inactive proconverting enzymes that are responsible for this processing cause profound obesity. Our laboratory demonstrated earlier that in the diet-induced obesity (DIO) state, the appetite-suppressing neuropeptide α-melanocyte-stimulating hormone (α-MSH) is reduced, yet the mRNA of its precursor protein proopiomelanocortin (POMC) remained unaltered. It was also shown that the DIO condition promotes the development of endoplasmic reticulum (ER) stress and leptin resistance. In the current study, using an in vivo model combined with in vitro experiments, we demonstrate that obesity-induced ER stress obstructs the post-translational processing of POMC by decreasing proconverting enzyme 2, which catalyzes the conversion of adrenocorticotropin to α-MSH, thereby decreasing α-MSH peptide production. This novel mechanism of ER stress affecting POMC processing in DIO highlights the importance of ER stress in regulating central energy balance in obesity.

Indexed as

Endoplasmic Reticulum StressProtein Processing, Post-TranslationalAdrenocorticotropic Hormonealpha-MSHAnimalsArcuate Nucleus of HypothalamusCell LineDiet, High-FateIF-2 KinaseEndoplasmic ReticulumGene Expression RegulationLeptinMaleMiceObesityPro-OpiomelanocortinAdrenocorticotropic Hormonealpha-MSHeIF-2 KinaseLeptinPro-OpiomelanocortinProprotein Convertase 2Protein Tyrosine Phosphatase, Non-Receptor Type 1Ptpn1 protein, ratSocs3 protein, ratSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling ProteinsEndoplasmic Reticulum StressEnergy MetabolismHypothalamusNeuropeptideProtein Processing

Identifiers

PMID23640886
PMCPMC3682568
OpenAlexW2085712839

What OpenQuestion 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 OpenQuestion graph.