ArticlePloS one2010
A common CNR1 (cannabinoid receptor 1) haplotype attenuates the decrease in HDL cholesterol that typically accompanies weight gain.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Meta-analyses between 18 candidate genetic markers and overweight/obesity.Diagnostic pathology · 2014Pooled it
- Cardiovascular effects of marijuana and synthetic cannabinoids: the good, the bad, and the ugly.Nature reviews. Cardiology · 2018Review
- The Endocannabinoid System and Heart Disease: The Role of Cannabinoid Receptor Type 2.Cardiovascular & hematological disorders drug targets · 2018Review
- Cannabinoid receptor signaling regulates liver development and metabolism.Development (Cambridge, England) · 2016Article
- Desiderata for computable representations of electronic health records-driven phenotype algorithms.Journal of the American Medical Informatics Association : JAMIA · 2015Article
- Secondary use of clinical data: the Vanderbilt approach.Journal of biomedical informatics · 2014Article
- A common functional promoter variant links CNR1 gene expression to HDL cholesterol level.Nature communications · 2013Article
- Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
We have previously shown that genetic variability in CNR1 is associated with low HDL dyslipidemia in a multigenerational obesity study cohort of Northern European descent (209 families, median = 10 individuals per pedigree). In order to assess the impact of CNR1 variability on the development of dyslipidemia in the community, we genotyped this locus in all subjects with class III obesity (body mass index >40 kg/m(2)) participating in a population-based biobank of similar ancestry. Twenty-two haplotype tagging SNPs, capturing the entire CNR1 gene locus plus 15 kb upstream and 5 kb downstream, were genotyped and tested for association with clinical lipid data. This biobank contains data from 645 morbidly obese study subjects. In these subjects, a common CNR1 haplotype (H3, frequency 21.1%) is associated with fasting TG and HDL cholesterol levels (p = 0.031 for logTG; p = 0.038 for HDL-C; p = 0.00376 for log[TG/HDL-C]). The strength of this relationship increases when the data are adjusted for age, gender, body mass index, diet and physical activity. Mean TG levels were 160±70, 155±70, and 120±60 mg/dL for subjects with 0, 1, and 2 copies of the H3 haplotype. Mean HDL-C levels were 45±10, 47±10, and 48±9 mg/dL, respectively. The H3 CNR1 haplotype appears to exert a protective effect against development of obesity-related dyslipidemia.
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Identifiers
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Registered trials
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.