Evidence map›Paper›PMID 33200240›Full record

ReviewDiabetologia2021

Brain JNK and metabolic disease.

Rubén Nogueiras, Guadalupe Sabio

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Diabetologia, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.4field-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

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
  3. Attack of the kinases: JNK signaling in metabolism.American journal of physiology. Regulatory, integrative and comparative physiology · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
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  12. Oral Administration of Efavirenz Dysregulates thePharmaceuticals (Basel, Switzerland) · 2024
    Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Lnc90386 Sponges miR-33-5p to MediateFrontiers in immunology · 2022
    Article
  20. 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

2 authors at 2 institutions in 1 country.

Rubén NogueirasDepartment of Physiology, Center for Research in Molecular Medicine and Chronic Diseases (CIMUS), University of Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain.
Guadalupe SabioDepartment of Myocardial Pathophysiology, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain. guadalupe.sabio@cnic.es.
Instituto de Investigación Sanitaria de Santiago · ESSpanish National Centre for Cardiovascular Research · ES

Funding

2017 Leonardo Grant for Researchers and Cultural Creators, BBVA Foundation IN[17]_BBM_BAS_0066AGENCIA ESTATAL DE INVESTIGACION RTI2018-099413-B-I00Comunidad de Madrid IMMUNOTHERCAN-CM S2010/BMD-2326 and B2017/BMD-3733ERC Synergy Grant-2019 810331European Foundation for the Study of Diabetes (EFSD) PO069European Union's Seventh Framework Programme (FP7/2007-2013) 260464MINECO-FEDER SAF2016-79126-RMINECO Severo Ochoa Center of Excellence SEV-2015-0505
6 · The paper itself

Abstract

Obesity, which has long since reached epidemic proportions worldwide, is associated with long-term stress to a variety of organs and results in diseases including type 2 diabetes. In the brain, overnutrition induces hypothalamic stress associated with the activation of several signalling pathways, together with central insulin and leptin resistance. This central action of nutrient overload appears very rapidly, suggesting that nutrition-induced hypothalamic stress is a major upstream initiator of obesity and associated diseases. The cellular response to nutrient overload includes the activation of the stress-activated c-Jun N-terminal kinases (JNKs) JNK1, JNK2 and JNK3, which are widely expressed in the brain. Here, we review recent findings on the regulation and effects of these kinases, with particular focus on the hypothalamus, a key brain region in the control of energy and glucose homeostasis. JNK1 blocks the hypothalamic-pituitary-thyroid axis, reducing energy expenditure and promoting obesity. Recently, opposing roles have been identified for JNK1 and JNK3 in hypothalamic agouti gene-related protein (AgRP) neurons: while JNK1 activation in AgRP neurons induces feeding and weight gain and impairs insulin and leptin signalling, JNK3 (also known as MAPK10) deletion in the same neuronal population produces very similar effects. The opposing roles of these kinases, and the unknown role of hypothalamic JNK2, reflect the complexity of JNK biology. Future studies should address the specific function of each kinase, not only in different neuronal subsets, but also in non-neuronal cells in the central nervous system. Decoding the puzzle of brain stress kinases will help to define the central stimuli and mechanisms implicated in the control of energy balance. Graphical abstract.

Indexed as

Agouti-Related ProteinAnimalsBrainEndoplasmic Reticulum StressEnergy MetabolismFeeding BehaviorGlucoseHumansHypothalamo-Hypophyseal SystemHypothalamusInsulinJNK Mitogen-Activated Protein KinasesLeptinMetabolic DiseasesMitogen-Activated Protein Kinase 10Mitogen-Activated Protein Kinase 8Agouti-Related ProteinGlucoseInsulinJNK Mitogen-Activated Protein KinasesLeptinMitogen-Activated Protein Kinase 10Mitogen-Activated Protein Kinase 8Mitogen-Activated Protein Kinase 9CNSDiabetesJNKKinasesMetabolismObesityPhosphorylationReviewSAPKSignallingStress

Identifiers

PMID33200240
OpenAlexW3100949868

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.