ArticleJournal, genetic engineering & biotechnology2026
Association of circulating leptin concentration with the risk of Clostridium difficile colitis and exploration of their associated mediators: A mendelian randomisation study.
Article in Journal, genetic engineering & biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundClostridioides difficile infection (CDI) is a leading cause of nosocomial diarrhea and colitis, imposing a significant burden. This study aims to elucidate the causal relationship between leptin and Clostridium difficile colitis and identify potential molecular mediators.
methodsUsing genome-wide association study (GWAS) summary statistics from the MRC Integrative Epidemiology Unit (MRC-IEU), we performed univariable and multivariable Mendelian randomization (MR) analyses, with inverse variance weighted (IVW) as the primary estimator, supplemented by weighted median, MR-Egger, and maximum likelihood methods. We also conducted linkage disequilibrium score regression (LDSC) to assess genetic correlations and two-step mediation MR to explore potential mediators. Multiple sensitivity analyses and Steiger tests ensured result robustness.
resultsGenetically predicted circulating leptin levels were associated with an increased risk of Clostridium difficile colitis (OR 2.456; 95% CI 1.231-4.90; P = 0.011). This association persisted in multivariable MR analyses incorporating adiponectin and resistin (OR 2.146; 95% CI 1.551-2.740; P = 0.012), and LDSC analysis revealed a genetic correlation between them (Rg = -0.521, Rg_SE = 0.599). Our mediation analysis indicated that leptin indirectly influenced CDI through "cholesterol in small dense LDL" (mediation proportion -2.99), "PTHrP" (mediation proportion -16.1%), and "TPST2" (mediation proportion -25.44%).
conclusionOur findings demonstrate an effect of genetically predicted circulating leptin levels on Clostridium difficile colitis risk. Furthermore, we identified cholesterol in small dense LDL, PTHrP, and TPST2 as potential molecular mediators, providing insights into the underlying pathophysiological mechanisms.
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