Evidence map›Paper›PMID 42158822›Full record

ArticleInternational journal of medical sciences2026

Insulin increases expression of cannabinoid receptor 1 by suppressing lysosomal degradation via ERK signaling pathway.

Shui-Yu Liu, Ching-Heng Ting, Guey-Shyang Hwang, Chien-Wei Chen, Luen-Kui Chen, Pin-Hsuan Ho, Pin-Hsuan Lee, Guan-Lin Wu, Wei-Hsian Yin, Liang-Yi Wu and 3 more

Abstract read
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Article in International journal of medical sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Shui-Yu LiuInstitute of Physiology, College of Medicine, National Yang Ming Chiao Tung University, Taipei 112304, Taiwan.
Ching-Heng TingInstitute of Physiology, College of Medicine, National Yang Ming Chiao Tung University, Taipei 112304, Taiwan.
Guey-Shyang HwangDepartment of Nursing, Chang Gung University of Science and Technology, Taoyuan 333324, Taiwan.
Chien-Wei ChenDepartment of Physical Education, Health, and Recreation, Teachers College, National Chiayi University, Chiayi 621302, Taiwan.
Luen-Kui ChenInstitute of Physiology, College of Medicine, National Yang Ming Chiao Tung University, Taipei 112304, Taiwan.
Pin-Hsuan HoInstitute of Physiology, College of Medicine, National Yang Ming Chiao Tung University, Taipei 112304, Taiwan.
Pin-Hsuan LeeInstitute of Physiology, College of Medicine, National Yang Ming Chiao Tung University, Taipei 112304, Taiwan.
Guan-Lin WuInstitute of Physiology, College of Medicine, National Yang Ming Chiao Tung University, Taipei 112304, Taiwan.
Wei-Hsian YinDivision of Cardiology, Cheng-Hsin General Hospital, Taipei 112401, Taiwan.
Liang-Yi WuDepartment of Bioscience Technology, College of Science, Chung-Yuan Christian University, Chung Li 320314, Taiwan.
Kok-Min SeowDepartment of Obstetrics and Gynecology, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei 111045, Taiwan.
Heng-Fu LinDivision of Trauma, Department of Surgery, Far-Eastern Memorial Hospital, New Taipei City 220216, Taiwan.
Chi-Chang JuanInstitute of Physiology, College of Medicine, National Yang Ming Chiao Tung University, Taipei 112304, Taiwan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Overactivation of the endocannabinoid (EC) system is an important pathogenic factor in the development of obesity. The inactivation of the EC system through administration of cannabinoid receptor 1 (CB1R) antagonist or CB1R knockout can ameliorate obesity-associated metabolic disorders such as insulin resistance and compensatory hyperinsulinemia and hepatic steatosis. However, the specific mechanisms by which hyperinsulinemia drives the progression of metabolic dysfunction-associated steatotic liver disease (MASLD) through CB1R remains poorly understood. The purpose of this study was to investigate the mechanism by which insulin regulates CB1R expression in hepatocytes. We studied the time and dose effects of insulin on CB1R expression in AML12 hepatocytes. Using specific inhibitors that act on insulin signaling pathways, we clarified the involvement of downstream signaling molecules in insulin-regulated CB1R expression. We also studied the effects of insulin on CB1R mRNA expression using real-time RT-PCR assays. In an

Indexed as

Fatty LiverHyperinsulinismInsulinReceptor, Cannabinoid, CB1AnimalsHepatocytesHumansInsulin ResistanceLiverLysosomesMaleMAP Kinase Signaling SystemMiceObesityRatsInsulinReceptor, Cannabinoid, CB1cannabinoid receptor 1ERKhepatocytesinsulinlysosomal pathway

Identifiers

PMID42158822
PMCPMC13181381

What OpenQuestion holds

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Registered trials

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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.