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BackgroundLipoma, a benign tumor derived from mesenchymal tissue, significantly affects patients’ physical and psychological wellbeing. Increasing evidence points to a strong link between the gut microbiome (GM) and lipoma incidence. This study utilizes Mendelian Randomization (MR) to assess the potential causal relationships between the GM and lipoma development.MethodsWe conducted a two-sample MR analysis using genome-wide association study (GWAS) data from MiBioGen and FinnGen to explore the causal relationship between GM and lipoma. The GM dataset included 18,340 participants with 14,587 single nucleotide polymorphisms (SNPs), while the lipoma dataset comprised 412,181 participants with 21,306,349 SNPs. We employed 5 MR methods: Inverse Variance Weighted (IVW), Weighted Median, Simple Mode, MR-Egger, and Weighted Mode. Additional assessments included Cochran’s Q test for result heterogeneity, PRESSO analysis for horizontal pleiotropy, and sensitivity analyses through scatter plots, leave-one-out analyses, funnel plots, and forest plots.ResultsThe IVW method identified 18 gene predictors trans-genus associated with lipoma risk. Protective effects against benign lipoma (BL) were observed in the Eubacterium rectale group, Desulfovibrio, Ruminococcus1, Clostridium sensu stricto1, and Lachnospiraceae UCG001; conversely, Lachnospiraceae UCG008 was linked to increased BL risk. Desulfovibrio provided protection against TS-BL; however, the Family XIII AD3011 group, Eubacterium coprostanoligenes group, Lachnospiraceae NK4A136 group, and Parasutterella were associated with an increased TS-BL risk. The Clostridium innocuum group, Eubacterium rectale group, Anaerotruncus, Ruminiclostridium6, and Lachnospiraceae UCG001 offered protection against LS-BL, while Lachnospiraceae UCG008 was linked to an increased LS-BL risk. The Eubacterium brachy group, Odoribacter, Butyricimonas, Subdoligranulum, and Clostridium sensu stricto1 were protective against HFNS-BL; Ruminococcaceae UCG005 was associated with an increased HFNS-BL risk.ConclusionCompared to malignant tumors, research on lipomas has been relatively limited. This study, through MR analysis, provided new evidence of a causal relationship between specific GM and the development of lipomas. Certain gut bacterial species may act as protective or harmful factors in lipoma formation, offering new avenues for future treatment strategies. However, additional research is required to unravel the complexity of how GM influences the pathogenesis of lipomas.
BackgroundLipoma, a benign tumor derived from mesenchymal tissue, significantly affects patients’ physical and psychological wellbeing. Increasing evidence points to a strong link between the gut microbiome (GM) and lipoma incidence. This study utilizes Mendelian Randomization (MR) to assess the potential causal relationships between the GM and lipoma development.MethodsWe conducted a two-sample MR analysis using genome-wide association study (GWAS) data from MiBioGen and FinnGen to explore the causal relationship between GM and lipoma. The GM dataset included 18,340 participants with 14,587 single nucleotide polymorphisms (SNPs), while the lipoma dataset comprised 412,181 participants with 21,306,349 SNPs. We employed 5 MR methods: Inverse Variance Weighted (IVW), Weighted Median, Simple Mode, MR-Egger, and Weighted Mode. Additional assessments included Cochran’s Q test for result heterogeneity, PRESSO analysis for horizontal pleiotropy, and sensitivity analyses through scatter plots, leave-one-out analyses, funnel plots, and forest plots.ResultsThe IVW method identified 18 gene predictors trans-genus associated with lipoma risk. Protective effects against benign lipoma (BL) were observed in the Eubacterium rectale group, Desulfovibrio, Ruminococcus1, Clostridium sensu stricto1, and Lachnospiraceae UCG001; conversely, Lachnospiraceae UCG008 was linked to increased BL risk. Desulfovibrio provided protection against TS-BL; however, the Family XIII AD3011 group, Eubacterium coprostanoligenes group, Lachnospiraceae NK4A136 group, and Parasutterella were associated with an increased TS-BL risk. The Clostridium innocuum group, Eubacterium rectale group, Anaerotruncus, Ruminiclostridium6, and Lachnospiraceae UCG001 offered protection against LS-BL, while Lachnospiraceae UCG008 was linked to an increased LS-BL risk. The Eubacterium brachy group, Odoribacter, Butyricimonas, Subdoligranulum, and Clostridium sensu stricto1 were protective against HFNS-BL; Ruminococcaceae UCG005 was associated with an increased HFNS-BL risk.ConclusionCompared to malignant tumors, research on lipomas has been relatively limited. This study, through MR analysis, provided new evidence of a causal relationship between specific GM and the development of lipomas. Certain gut bacterial species may act as protective or harmful factors in lipoma formation, offering new avenues for future treatment strategies. However, additional research is required to unravel the complexity of how GM influences the pathogenesis of lipomas.
Background: Recent studies have established associations between the gut microbiota (GM) and thyroid diseases (TDs). However, their causal relationships remain elusive. Methods: To investigate this causality, we conducted a two-sample Mendelian randomization (MR) analysis using genome-wide association study (GWAS) data from MiBioGen and FinnGen, with GM as the exposure and six TDs as outcomes. Results: We identified 32 microbial taxa linked to the risk of six TDs. The Clostridium innocuum group, Ruminiclostridium5, and Lachnoclostridium exhibited protective effects against nontoxic diffuse goiter (NDG). Conversely, an increased risk of NDG was associated with Ruminococcaceae UCG002, Alistipes, Methanobrevibacter, Marvinbryantia, and Ruminococcaceae UCG014. Bifidobacterium and Sutterella were protective against nontoxic multinodular goiter (NMG), while the Ruminococcus gauvreauii group and Rikenellaceae RC9 gut group heightened NMG risk. Protective effects against nontoxic single thyroid nodule (NSTN) were observed with Defluviitaleaceae UCG011, Ruminococcus1, and Ruminococcaceae UCG010, whereas increased risk was linked to Alistipes, the Ruminococcus gauvreauii group, and Lachnospiraceae UCG010. Ruminiclostridium9, Victivallis, and Butyricimonas offered protection against thyrotoxicosis with Graves’ Disease (GD), while the Eubacterium rectale group, Desulfovibrio, Bifidobacterium, Collinsella, Oscillospira, and Catenibacterium were risk factors. For thyrotoxicosis with Plummer Disease (PD), protective taxa included Butyricimonas and Lachnospira, whereas Dorea, Eggerthella, Odoribacter, Lactobacillus, Intestinimonas, and Phascolarctobacterium increased risk. Lastly, Parasutterella was protective against thyrotoxicosis with toxic single thyroid nodule (TSTN), while increased risk was associated with Sutterella, Oscillibacter, and Clostridium sensu stricto1. Conclusions: Our findings support a causal relationship between specific GM and TDs at the genetic level, laying the foundation for future research into potential mechanisms and the identification of novel therapeutic targets.
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