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As fatty acid biosynthesis is central to membrane structure and function, and <jats:styled-content style=\"fixed-case\"><jats:italic>H.\u2009pylori<\/jats:italic><\/jats:styled-content> is correlated with the erosion of the mucosal barrier, lipidome analysis can elucidate the role of fatty acid metabolism in <jats:styled-content style=\"fixed-case\"><jats:italic>H.\u2009pylori<\/jats:italic><\/jats:styled-content> infection and yield potential targets for intervention.<\/jats:p><\/jats:sec><jats:sec><jats:title>Materials and Methods<\/jats:title><jats:p>Fecal samples from 68 <jats:styled-content style=\"fixed-case\"><jats:italic>H.\u2009pylori<\/jats:italic><\/jats:styled-content> patients and 35 healthy control subjects were analyzed for fatty acid composition using gas chromatography\u2013mass spectrometry.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>We observed an increase in margaric acid\/17:0, eicosapentaenoic acid (EPA)\/20:5n3, erucic acid\/22:1n9, and docosapentaenoic acid (DPA)\/22:5n3 as well as eicosatetraenoic acid\/20:4n3 and docosahexaenoic acid (DHA)\/22:6n3 in <jats:styled-content style=\"fixed-case\"><jats:italic>H.\u2009pylori<\/jats:italic><\/jats:styled-content> patients relative to the healthy control subjects. In contrast, the PUFAs gamma\u2010linolenic acid\/18:3n6 and osbond acid\/22:5n6 were decreased in the <jats:styled-content style=\"fixed-case\"><jats:italic>H.\u2009pylori<\/jats:italic><\/jats:styled-content> patients relative to healthy controls. Most of the fatty acids that differ in quantity between <jats:styled-content style=\"fixed-case\"><jats:italic>H.\u2009pylori<\/jats:italic><\/jats:styled-content>\u2010positive samples and controls are metabolites of omega\u20103 and omega\u20106 fatty acid metabolism. Smoking, alcohol use, and non\u2010ulcer dyspepsia further influenced fatty acid metabolism during <jats:styled-content style=\"fixed-case\"><jats:italic>H.\u2009pylori<\/jats:italic><\/jats:styled-content> infection.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Here, we propose a model for the pathophysiology of <jats:styled-content style=\"fixed-case\"><jats:italic>H.\u2009pylori<\/jats:italic><\/jats:styled-content> infection based on the gut lipid signatures of <jats:styled-content style=\"fixed-case\"><jats:italic>H.\u2009pylori<\/jats:italic><\/jats:styled-content> patients and healthy control subjects. Our results may provide insight on how <jats:styled-content style=\"fixed-case\"><jats:italic>H.\u2009pylori<\/jats:italic><\/jats:styled-content> infection leads to changes in fatty acid metabolism, how the host responds, and which metabolites may serve as potential candidates for future interventions.<\/jats:p><\/jats:sec>","DOI":"10.1111\/hel.70060","type":"journal-article","created":{"date-parts":[[2025,8,5]],"date-time":"2025-08-05T12:07:32Z","timestamp":1754395652000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Lipidome Characterization Reveals Alterations of Fatty Acid Metabolism in <scp><i>Helicobacter pylori<\/i><\/scp> Infection"],"prefix":"10.1111","volume":"30","author":[{"given":"Hyder","family":"Alikhan","sequence":"first","affiliation":[{"name":"Department of Biomedical Sciences Cooper Medical School of Rowan University  Camden New Jersey 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