{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T05:19:44Z","timestamp":1774415984720,"version":"3.50.1"},"reference-count":20,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2018,7,30]],"date-time":"2018-07-30T00:00:00Z","timestamp":1532908800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Neurogastroenterology Motil"],"published-print":{"date-parts":[[2018,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>The mechanism by which obesity leads to damage independent of reflux is unclear. We aimed to determine the influence of obesity on mean nocturnal baseline impedance (<jats:styled-content style=\"fixed-case\">MNBI<\/jats:styled-content>), a functional measure of the epithelial barrier, in the presence and absence of acid reflux, using ambulatory <jats:styled-content style=\"fixed-case\">pH<\/jats:styled-content> impedance measurements.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Twenty\u2010four\u2010hour <jats:styled-content style=\"fixed-case\">pH<\/jats:styled-content> impedance studies performed off medications in Caucasian men with a normal endoscopic examination were assessed for level of acid exposure and <jats:styled-content style=\"fixed-case\">MNBI<\/jats:styled-content>. Four patient groups were studied: Group 1, Not obese and normal acid exposure; Group 2, Obese and normal acid exposure; Group 3, Not obese and increased acid exposure; and Group 4, Obese with increased acid exposure.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>One hundred patients were studied (25 in each group). Mean esophageal mucosal impedance (<jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>) was substantially lower in obese patients without reflux (Group 2) and non\u2010obese patients with reflux (Group 3) compared to normal controls (non\u2010obese, no reflux, Group 1). <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content> was progressively lower in the distal (vs the proximal) esophagus in <jats:styled-content style=\"fixed-case\">GER<\/jats:styled-content> patients, compared to those without <jats:styled-content style=\"fixed-case\">GER<\/jats:styled-content>. This difference persisted in the presence or absence of obesity. In contrast, in obese patients, the mean <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content> was significantly lower throughout the esophagus when compared to the non\u2010obese patients and also persisted in the presence and absence of accompanying reflux. Obesity and reflux were both independently negatively correlated with <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Obesity is associated with abnormal esophageal <jats:styled-content style=\"fixed-case\">MNBI<\/jats:styled-content>. In contrast to gastro\u2010esophageal reflux, this decrease is pan\u2010esophageal. These data may support a systemic mechanism by which obesity alters the esophageal barrier function.<\/jats:p><\/jats:sec>","DOI":"10.1111\/nmo.13403","type":"journal-article","created":{"date-parts":[[2018,7,31]],"date-time":"2018-07-31T05:15:20Z","timestamp":1533014120000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["Obesity and <scp>GERD<\/scp> impair esophageal epithelial permeability through 2 distinct mechanisms"],"prefix":"10.1111","volume":"30","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0192-3363","authenticated-orcid":false,"given":"C. H.","family":"Blevins","sequence":"first","affiliation":[{"name":"Division of Gastroenterology and Hepatology Mayo Clinic Minnesota  Rochester MN USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R. A.","family":"Dierkhising","sequence":"additional","affiliation":[{"name":"Division of Biomedical Statistics and Informatics Mayo Clinic Minnesota  Rochester MN USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D. M.","family":"Geno","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology Mayo Clinic Minnesota  Rochester MN USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M. L.","family":"Johnson","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology Mayo Clinic Minnesota  Rochester MN USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M. F.","family":"Vela","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology Mayo Clinic Arizona  Scottsdale AZ USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K.","family":"Ravi","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology Mayo Clinic Minnesota  Rochester MN USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P. G.","family":"Iyer","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology Mayo Clinic Minnesota  Rochester MN USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D. 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