Evidence mapPaperPMID 36964619Full record

ArticleBiological research2023

The CB1 cannabinoid receptor regulates autophagy in the tibialis anterior skeletal muscle in mice.

Carlos Sepúlveda, Juan Manuel Rodríguez, Matías Monsalves-Álvarez, Camila Donoso-Barraza, Francisco Pino-de la Fuente, Isabelle Matías, Thierry Leste-Lasserre, Philippe Zizzari, Eugenia Morselli, Daniela Cota and 2 more

Open access · goldFull text read
In one paragraph

Article in Biological research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

3 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. 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

12 authors at 6 institutions in 2 countries.

Carlos SepúlvedaLaboratorio de Investigación en Nutrición y Actividad Física (LABINAF), Instituto de Nutrición y Tecnología de los Alimentos (INTA), Universidad de Chile, Santiago, Chile. csepulvedag@ug.uchile.cl.
Juan Manuel RodríguezLaboratorio de Investigación en Nutrición y Actividad Física (LABINAF), Instituto de Nutrición y Tecnología de los Alimentos (INTA), Universidad de Chile, Santiago, Chile.
Matías Monsalves-ÁlvarezUniversidad de O'Higgins, Rancagua, Chile.
Camila Donoso-BarrazaLaboratorio de Investigación en Nutrición y Actividad Física (LABINAF), Instituto de Nutrición y Tecnología de los Alimentos (INTA), Universidad de Chile, Santiago, Chile.
Francisco Pino-de la FuenteLaboratorio de Investigación en Nutrición y Actividad Física (LABINAF), Instituto de Nutrición y Tecnología de los Alimentos (INTA), Universidad de Chile, Santiago, Chile.
Isabelle MatíasUniversity of Bordeaux, INSERM, Neurocentre Magendie, U1215, 33000, Bordeaux, France.
Thierry Leste-LasserreUniversity of Bordeaux, INSERM, Neurocentre Magendie, U1215, 33000, Bordeaux, France.
Philippe ZizzariUniversity of Bordeaux, INSERM, Neurocentre Magendie, U1215, 33000, Bordeaux, France.
Eugenia MorselliDepartment of Basic Sciences, Faculty of Medicine and Sciences, Universidad San Sebastián, Santiago de Chile, Chile.
Daniela CotaUniversity of Bordeaux, INSERM, Neurocentre Magendie, U1215, 33000, Bordeaux, France.
Miguel LlanosLaboratorio de Investigación en Nutrición y Actividad Física (LABINAF), Instituto de Nutrición y Tecnología de los Alimentos (INTA), Universidad de Chile, Santiago, Chile.
Rodrigo TroncosoLaboratorio de Investigación en Nutrición y Actividad Física (LABINAF), Instituto de Nutrición y Tecnología de los Alimentos (INTA), Universidad de Chile, Santiago, Chile. rtroncoso@inta.uchile.cl.ORCID http://orcid.org/0000-0003-0796-5908
Université de Bordeaux · FRUniversity of Chile · CLUniversity of O'Higgins · CLAdvanced Center for Chronic Diseases · CLClínica MEDS (Chile) · CLSan Sebastián University · CL

Funding

Agencia Nacional de Investigación y Desarrollo FONDECYT 1191078
6 · The paper itself

Abstract

The endocannabinoid system (ECS) regulates energy metabolism, has been implicated in the pathogenesis of metabolic diseases and exerts its actions mainly through the type 1 cannabinoid receptor (CB1). Likewise, autophagy is involved in several cellular processes. It is required for the normal development of muscle mass and metabolism, and its deregulation is associated with diseases. It is known that the CB1 regulates signaling pathways that control autophagy, however, it is currently unknown whether the ECS could regulate autophagy in the skeletal muscle of obese mice. This study aimed to investigate the role of the CB1 in regulating autophagy in skeletal muscle. We found concomitant deregulation in the ECS and autophagy markers in high-fat diet-induced obesity. In obese CB1-KO mice, the autophagy-associated protein LC3 II does not accumulate when mTOR and AMPK phosphorylation levels do not change. Acute inhibition of the CB1 with JD-5037 decreased LC3 II protein accumulation and autophagic flux. Our results suggest that the CB1 regulates autophagy in the tibialis anterior skeletal muscle in both lean and obese mice.

Indexed as

CannabinoidsAnimalsAutophagyMiceMice, Inbred C57BLMice, ObeseMuscle, SkeletalReceptor, Cannabinoid, CB1CannabinoidsReceptor, Cannabinoid, CB1AutophagyEndocannabinoid receptorHigh-fat dietSkeletal muscle

Identifiers

PMID36964619
PMCPMC10039507
OpenAlexW4360939549

What Socratic holds

Textfull text, public
LicenceCC BY
reference markers read2
measurements read42
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.