Evidence suggests there might be a causal relationship between high serum adiponectin and a decreased risk of developing idiopathic pulmonary fibrosis (IPF), however, adipokines such as leptin, resistin, or monocyte chemoattractant protein-1 (MCP-1) appear unrelated to the risk of IPF, according to a study published in Lung.
The researchers analyzed the summary data from genome-wide association studies regarding adiponectin, leptin, resistin, MCP-1, and IPF. They used the inverse-variance weighted method as well as the Mendelian randomization-Egger, weighted median, simple mode, and weighted mode methods. They also included sensitivity analyses such as the heterogeneity test, horizontal pleiotropy test, and leave-one-out analysis.
According to the results, the causal effect of the circulating adiponectin levels might decrease the risk of developing IPF. No causal associations were identified for genetic changes in serum leptin, resistin, or MCP-1. The selected number of single nucleotide polymorphisms was 13 for adiponectin, 6 for leptin, 12 for resistin, and 6 for MCP-1.
No evidence showed heterogeneity or horizontal pleiotropy. The sensitivity analyses confirmed the stability and reliability of the study results.
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“Although the exact mechanisms by which adipokines contribute to IPF are unknown, current data suggest that a persistent elevation of adipokines might increase susceptibility to IPF via the aberrant innate and adaptive immune responses and the chronic inflammation,” Huang and colleagues noted.
Adiponectin, the most abundant of all adipokines, correlates negatively with adiposity and exhibits strong intense anti-insulin, anti-inflammatory, antiapoptotic, and antifibrotic properties. It is also a messenger between the adipose tissues and multiple systemic organs.
Huang D, Gong L, Wu Z, Shi Y, Liang Z. Genetic association of circulating adipokines with risk of idiopathic pulmonary fibrosis: a two-sample Mendelian randomization study. Lung. Published online August 2, 2023. doi:10.1007/s00408-023-00640-8