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Mechanistic validation was performed using in\u00a0vitro and in\u00a0vivo\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>H. pylori<\/jats:italic>\n                      <\/jats:styled-content>\n                      PMSS1 infection models, combined with single\u2010cell RNA sequencing, molecular analyses, histopathology, and lipidomics.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>Helicobacter pylori<\/jats:italic>\n                      <\/jats:styled-content>\n                      infection was associated with increased LDL cholesterol and triglycerides, reduced HDL cholesterol, and elevated NHHR, which independently predicted hyperlipidemia risk. At the mechanistic level,\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>H. pylori<\/jats:italic>\n                      <\/jats:styled-content>\n                      infection consistently suppressed gastric expression of Gpihbp1, a key mediator of lipoprotein lipase\u2013dependent lipid transport. Infected mice developed systemic hyperlipidemia and exhibited lipidomic remodeling characterized by glycerolipid accumulation and reduced phosphatidylcholine species. Importantly, genetic deficiency of\n                      <jats:italic>Gpihbp1<\/jats:italic>\n                      promoted gastric\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>H. pylori<\/jats:italic>\n                      <\/jats:styled-content>\n                      colonization and exacerbated mucosal inflammation, revealing a reciprocal interaction between host lipid metabolism and bacterial persistence.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      These findings define a microbiota\u2013host lipid transport axis linking chronic\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>H. pylori<\/jats:italic>\n                      <\/jats:styled-content>\n                      infection to dyslipidemia and suggest that integrated targeting of microbial infection and metabolic dysfunction may offer therapeutic benefit.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/hel.70135","type":"journal-article","created":{"date-parts":[[2026,5,16]],"date-time":"2026-05-16T08:47:52Z","timestamp":1778921272000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["A Bidirectional Association Between\n                    <i>Helicobacter pylori<\/i>\n                    Infection and Hyperlipidemia: Clinical Evidence and Mechanistic Insights"],"prefix":"10.1111","volume":"31","author":[{"given":"Yan'an","family":"Zhou","sequence":"first","affiliation":[{"name":"Jiangxi Provincial Key Laboratory of Digestive Diseases, Department of Gastroenterology, Digestive Disease Hospital The First Affiliated Hospital, Jiangxi Medical College, Nanchang University  Nanchang Jiangxi China"},{"name":"Department of Cardiology The 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