Evidence map›Paper›PMID 20835701›Full record

ArticleDiabetologia2010

Deficiency of CB2 cannabinoid receptor in mice improves insulin sensitivity but increases food intake and obesity with age.

J Agudo, M Martin, C Roca, M Molas, A S Bura, A Zimmer, F Bosch, R Maldonado

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 2 pooled it
6.2field-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

67 citing papers in PubMed, 2 syntheses or guidelines pooled it, 117 citations in OpenAlex.

  1. The Role of Cannabidiol in Liver Disease: A Systemic Review.International journal of molecular sciences · 2024
    Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Review
  6. Review
  7. Cannabinoids and the endocannabinoid system in liver diseases.Clinical and experimental hepatology · 2024
    Review
  8. Review
  9. The Impact of the CBMolecules (Basel, Switzerland) · 2024
    Review
  10. Article
  11. Review
  12. The Role of the Endocannabinoid System in Binge Eating Disorder.International journal of molecular sciences · 2023
    Review
  13. Treatment of Diet-Induced Obese Rats with CBInternational journal of molecular sciences · 2023
    Article
  14. Article
  15. Review
  16. Article
  17. Cannabinoids and Chronic Liver Diseases.International journal of molecular sciences · 2022
    Review
  18. Article
  19. Review
  20. Article

7 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

8 authors at 4 institutions in 2 countries.

J AgudoCenter of Animal Biotechnology and Gene Therapy, Department of Biochemistry and Molecular Biology, School of Veterinary Medicine, Universitat Autònoma de Barcelona, Bellaterra, Spain.
M Martin
C Roca
M Molas
A S Bura
A Zimmer
F Bosch
R Maldonado
Pompeu Fabra University · ESUniversitat Autònoma de Barcelona · ESCentro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas · ESUniversity of Bonn · DE

Funding

VULNERABILITY TO NICOTINE ADDICTIONR01DA016768 · NIDA · POMPEU FABRA UNIVERSITY · PI MALDONADO, RAFAEL · 2004 to 2008
$1.5M
NIDA NIH HHS 5R01-DA016768
6 · The paper itself

Abstract

aims/hypothesisThe endocannabinoid system has a key role in energy storage and metabolic disorders. The endocannabinoid receptor 2 (CB2R), which was first detected in immune cells, is present in the main peripheral organs responsible for metabolic control. During obesity, CB2R is involved in the development of adipose tissue inflammation and fatty liver. We examined the long-term effects of CB2R deficiency in glucose metabolism.

methodsMice deficient in CB2R (Cb2 ( -/- ) [also known as Cnr2]) were studied at different ages (2-12 months). Two-month-old Cb2 (-/-) and wild-type mice were treated with a selective CB2R antagonist or fed a high-fat diet.

resultsThe lack of CB2R in Cb2 (-/-) mice led to greater increases in food intake and body weight with age than in Cb2 (+/+) mice. However, 12-month-old obese Cb2 (-/-) mice did not develop insulin resistance and showed enhanced insulin-stimulated glucose uptake in skeletal muscle. In agreement, adipose tissue hypertrophy was not associated with inflammation. Similarly, treatment of wild-type mice with CB2R antagonist resulted in improved insulin sensitivity. Moreover, when 2-month-old Cb2 (-/-) mice were fed a high-fat diet, reduced body weight gain and normal insulin sensitivity were observed. CONCLUSIONS/

interpretationThese results indicate that the lack of CB2R-mediated responses protected mice from both age-related and diet-induced insulin resistance, suggesting that these receptors may be a potential therapeutic target in obesity and insulin resistance.

Indexed as

3T3-L1 CellsAdipose TissueAgingAnimalsEatingGenetic Predisposition to DiseaseInsulin ResistanceIon ChannelsMaleMiceMice, Inbred C57BLMice, KnockoutMitochondrial ProteinsObesityReceptor, Cannabinoid, CB2Uncoupling Protein 1Ion ChannelsMitochondrial ProteinsReceptor, Cannabinoid, CB2Uncoupling Protein 1

Identifiers

PMID20835701
OpenAlexW1999074163

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.