{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,7]],"date-time":"2026-05-07T21:39:21Z","timestamp":1778189961739,"version":"3.51.4"},"reference-count":34,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2024,2,11]],"date-time":"2024-02-11T00:00:00Z","timestamp":1707609600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Neurogastroenterology Motil"],"published-print":{"date-parts":[[2024,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Altered prandial glycemic response after Roux\u2010en\u2010Y gastric bypass (RYGB) is exaggerated in patients with post\u2010RYGB hypoglycemia. Increased contribution of glucagon\u2010like peptide 1 (GLP\u20101) to prandial insulin secretion plays a key role in developing hypoglycemia after RYGB, but the role of nonhormonal gut factors remains unknown. Here, the effect of vagal activation on prandial bile acid (BA) composition in relation to glucose, insulin and gut hormone responses was examined in a small size group of nondiabetic subjects after RYGB with intact gallbladder compared to nonoperated controls.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Concentrations of blood glucose, hormones, and BAs were measured in two RYGB subjects with documented hypoglycemia (HGB), three asymptomatic RYGB\u2010treated subjects (AGB), and four nonoperated controls with intact gallbladders during a meal\u2010tolerance test with (MTT\u2010Sham) and without (MTT) preceding modified sham feeding (chew and spit).<\/jats:p><\/jats:sec><jats:sec><jats:title>Key Results<\/jats:title><jats:p>Meal ingestion raised serum total BAs in RYGB\u2010treated subjects without any effect in nonoperated controls. Modified sham feeding similarly increased meal\u2010induced responses of conjugated BAs (CBAs) in all subjects (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05 compared to MTT alone), whereas unconjugated BAs (UBAs), mainly deoxycholic and chenodeoxycholic acid, were raised only in the HGB group (<jats:italic>p\u2009&lt;<\/jats:italic>\u20090.001 for interaction). Prandial UBAs had an inverse correlation with glucose nadir (<jats:italic>r<\/jats:italic>\u2009=\u2009\u22120.75, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05) and were directly associated with ISR and GLP\u20101 during MTT\u2010Sham.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions &amp; Inferences<\/jats:title><jats:p>In this small cohort, vagal activation by modified sham feeding increases prandial CBAs in both operated and nonoperated subjects but enhances UBAs only in patients with documented post\u2010RYGB hypoglycemia. Our findings highlight a potential role for nonhormonal gut factors, such as BA and gut microbiome, in glucose abnormalities after RYGB.<\/jats:p><\/jats:sec>","DOI":"10.1111\/nmo.14763","type":"journal-article","created":{"date-parts":[[2024,2,12]],"date-time":"2024-02-12T04:23:40Z","timestamp":1707711820000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Vagal activation alters prandial bile acid composition and glycemia in patients with hypoglycemia after <scp>Roux\u2010en\u2010Y<\/scp> gastric bypass surgery"],"prefix":"10.1111","volume":"36","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1389-6355","authenticated-orcid":false,"given":"Henri","family":"Honka","sequence":"first","affiliation":[{"name":"Division of Diabetes University of Texas Health Science Center  San Antonio Texas USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jashdeep","family":"Bhattacharjee","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology, Hepatology and Nutrition Children's Hospital Los Angeles  Los Angeles California USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mansour","family":"Zadeh","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Immunology and Molecular Genetics University of Texas Health Science Center  San Antonio Texas USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rohit","family":"Kohli","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology, Hepatology and Nutrition Children's Hospital Los Angeles  Los Angeles California USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Amalia","family":"Gastaldelli","sequence":"additional","affiliation":[{"name":"Cardiometabolic Risk Unit Institute of Clinical Physiology\u2010National Research Council  Pisa Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marzieh","family":"Salehi","sequence":"additional","affiliation":[{"name":"Division of Diabetes University of Texas Health Science Center  San Antonio Texas USA"},{"name":"Department of Medicine University of Cincinnati College of Medicine  Cincinnati Ohio USA"},{"name":"South Texas Veterans Health Care System, Audie Murphy Hospital  San Antonio Texas 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