Higher adiponectin not tied with increased risk of asthma: Study
Higher adiponectin is not tied with increased risk of asthma according to genetic evidence published in recently in Thorax
Adiponectin, an adipocyte-secreted protein hormone with inflammatory properties, has a potentially important role in the development and progression of asthma. Unravelling whether adiponectin is a causal risk factor for asthma is an important issue to clarify as adiponectin could be a potential novel drug target for the treatment of asthma.
A group of researchers tested the hypothesis that plasma adiponectin is associated observationally and causally (using genetic variants as instrumental variables) with the risk of asthma.
In the Copenhagen General Population Study, we did an observational analysis in 28 845 individuals (2278 asthma cases) with plasma adiponectin measurements, and a genetic one-sample Mendelian randomisation analysis in 94 868 individuals (7128 asthma cases) with 4 genetic variants. Furthermore, in the UK Biobank, we did a genetic two-sample Mendelian randomisation analysis in 462 933 individuals (53 598 asthma cases) with 12 genetic variants. Lastly, we meta-analysed the genetic findings.
The Results of the study are as follows:
While a 1 unit log-transformed higher plasma adiponectin in the Copenhagen General Population Study was associated with an observational OR of 1.65 (95% CI 1.29 to 2.08) for asthma, the corresponding genetic causal OR was 1.03 (95% CI 0.75 to 1.42). The genetic causal OR for asthma in the UK Biobank was 1.00 (95% CI 0.99 to 1.00). Lastly, a genetic meta-analysis confirmed the lack of association between genetically high plasma adiponectin and causal OR for asthma.
Thus, the researchers concluded that observationally, high plasma adiponectin is associated with an increased risk of asthma; however, genetic evidence could not support a causal association between plasma adiponectin and asthma.
Reference:
Plasma adiponectin and risk of asthma: observational analysis, genetic Mendelian randomisation and meta-analysis by Maria Booth Nielsen et al. published in the Thorax.
https://pubmed.ncbi.nlm.nih.gov/34949725/
