Genetically Predicted Higher Levels of Caffeic Acid Are Protective Against Ulcerative Colitis: A Comprehensive Metabolome Analysis.

Background It is crucial to pinpoint the metabolites that cause Crohn's disease (CD) and ulcerative colitis (UC) to comprehend their pathogenesis and identify possible targets for therapy. To achieve this goal, we performed the first metabolome-wide Mendelian randomization (MR) study of Japanese pat...

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Publicado en:Inflammatory Bowel Diseases Vol. 30; no. 12; pp. 2440 - 2449
Autores principales: Naito, Takeo, Osaka, Ryuya, Kakuta, Yoichi, Kawai, Yosuke, Khor, Seik-Soon, Umeno, Junji, Tokunaga, Katsushi, Consortium, NCBN Controls WGS, Nagai, Hiroshi, Shimoyama, Yusuke, Moroi, Rintaro, Shiga, Hisashi, Nagasaki, Masao, Kinouchi, Yoshitaka, Masamune, Atsushi
Formato: research tables/charts Journal Article
Publicado: Oxford University Press / USA Dec2024
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Dec2024
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      pub: Oxford University Press / USA
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        10.1093/ibd/izae143
        181987481
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        atl: Genetically Predicted Higher Levels of Caffeic Acid Are Protective Against Ulcerative Colitis: A Comprehensive Metabolome Analysis.
      aug:
        au:
          Naito, Takeo
          Osaka, Ryuya
          Kakuta, Yoichi
          Kawai, Yosuke
          Khor, Seik-Soon
          Umeno, Junji
          Tokunaga, Katsushi
          Consortium, NCBN Controls WGS
          Nagai, Hiroshi
          Shimoyama, Yusuke
          Moroi, Rintaro
          Shiga, Hisashi
          Nagasaki, Masao
          Kinouchi, Yoshitaka
          Masamune, Atsushi
        affil: Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Japan
      sug:
        subj:
          Acids, Carbocyclic Therapeutic Use
          Colitis, Ulcerative Drug Therapy
          Crohn Disease Drug Therapy
          Metabolomics
          Mendelian Randomization
          Human
          Japan
          Metabolites
          Japanese Persons
          Descriptive Statistics
          Odds Ratio
          Tryptophan Therapeutic Use
          Colitis, Ulcerative Risk Factors
          Crohn Disease Risk Factors
          Causal Attribution
          Funding Source
      ab: Background It is crucial to pinpoint the metabolites that cause Crohn's disease (CD) and ulcerative colitis (UC) to comprehend their pathogenesis and identify possible targets for therapy. To achieve this goal, we performed the first metabolome-wide Mendelian randomization (MR) study of Japanese patients with CD and UC. Methods As exposure datasets, genetic instruments with blood-circulating metabolites were obtained from the Tohoku Medical Megabank Organization, which includes 204 metabolites from the genome-wide association study data of 7843 Japanese individuals. As outcome datasets, we enrolled Japanese patients with CD (n = 1803), Japanese patients with UC (n = 1992), and healthy controls (n = 2022). The main analysis utilized the inverse variance–weighted method, while stability of the findings was evaluated through sensitivity analyses. Results After single nucleotide polymorphism (SNP) filtering, 169 SNPs for 45 metabolites were available for MR. Genetically predicted elevated circulating trans-glutaconic acid and tryptophan were associated with a lower CD risk (odds ratio [OR], 0.68; P  = 5.95 × 10−3; and OR, 0.64; P  = 1.90 × 10−2, respectively). Genetically predicted elevated caffeic acid was associated with a lower UC risk (OR, 0.67; P  = 4.2 × 10−4), which remained significant after multiple testing correction. We identified a causal link between UC and 3-hydroxybutyrate (OR, 2.21; P  = 1.41 × 10−2), trans-glutaconic acid (OR, 0.72; P  = 1.77 × 10−2), and 2-hydroxyvaleric acid (OR, 1.31; P  = 4.23 × 10−2). There was no evidence of pleiotropy or reverse causal effects for these candidate metabolites. Conclusions In our metabolome-wide MR study, we discovered a notable protective effect of caffeic acid against UC.
      pubtype: Academic Journal
      doctype:
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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