ArticleBMJ open2019
Association between genetically determined leptin and blood lipids considering alcohol consumption: a Mendelian randomisation study.
Article in BMJ open, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Sources of Variability in Serum Lipidomic Measurements and Implications for Epidemiologic Studies.American journal of epidemiology · 2022Article
- Maternal obesity and ovarian failure: is leptin the culprit?Animal reproduction · 2022Article
- Four-Way Decomposition of Effect of Alcohol Consumption and Body Mass Index on Lipid Profile.International journal of environmental research and public health · 2021Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesThe objective of this study was to evaluate the association of genetically determined leptin with lipids.
designWe conducted a Mendelian randomisation study to assess a potential causal relationship between serum leptin and lipid levels. We also evaluated whether alcohol drinking modified the associations of genetically determined leptin with blood lipids. SETTING AND
participants3860 participants of the Framingham Heart Study third generation cohort.
resultsBoth genetic risk scores (GRSs), the GRS generated using leptin loci independent of body mass index (BMI) and GRS generated using leptin loci dependent of BMI, were positively associated with log-transformed leptin (log-leptin). The BMI-independent leptin GRS was associated with log-transformed triglycerides (log-TG, β=-0.66, p=0.01), but not low-density lipoprotein cholesterol (LDL-C, p=0.99), high-density lipoprotein cholesterol (HDL-C, p=0.44) or total cholesterol (TC, p=0.49). Instrumental variable estimation showed that per unit increase in genetically determined log-leptin was associated with 0.55 (95% CI: 0.05 to 1.00) units decrease in log-TG. Besides significant association with log-TG (β=-0.59, p=0.009), the BMI-dependent GRS was nominally associated with HDL-C (β=-10.67, p=0.09) and TC (β=-28.05, p=0.08). When stratified by drinking status, the BMI-dependent GRS was associated with reduced levels of LDL-C (p=0.03), log-TG (p=0.004) and TC (p=0.003) among non-current drinkers only. Significant interactions between the BMI-dependent GRS and alcohol drinking were identified for LDL-C (p=0.03), log-TG (p=0.03) and TC (p=0.02).
conclusionThese findings together indicated that genetically determined leptin was negatively associated with lipid levels and the association may be modified by alcohol consumption.
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