{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T23:44:21Z","timestamp":1792626261453,"version":"4.5.0"},"reference-count":34,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2022,5]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>Postural tachycardia syndrome (POTS) is characterized by excessive upright tachycardia and disabling presyncopal symptoms, which are exacerbated after consuming a high-carbohydrate meal; it is unknown, however, what is the precise underlying mechanism. We seek to investigate the effect of glucose intake on orthostatic hemodynamic changes and gastrointestinal hormone secretion in POTS.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>Prospective, case-control study, 12 women with POTS who reported a postprandial worsening of their POTS symptoms and 13 age-matched female controls received 75-g oral glucose and 20 mg\/kg acetaminophen to assess nutrient absorption. Hemodynamic, gastrointestinal hormone and acetaminophen levels were measured for up to 120 minutes postingestion while supine and standing.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      Patients with POTS had significant orthostatic tachycardia, 48.7\u00b111.2 versus 23.3\u00b18.1 bpm,\n                      <jats:italic>P<\/jats:italic>\n                      =0.012 and elevated upright norepinephrine levels, 835.2\u00b1368.4 versus 356.9\u00b1156.7 pg\/mL,\n                      <jats:italic>P<\/jats:italic>\n                      =0.004. After oral glucose, upright heart rate significantly increased in POTS, 21.2\u00b111.9% versus 6.0\u00b119.9%,\n                      <jats:italic>P<\/jats:italic>\n                      =0.033 with a concomitant decline in upright stroke volume, \u221210.3\u00b111.90% versus 3.3\u00b113.7%,\n                      <jats:italic>P<\/jats:italic>\n                      =0.027; total peripheral resistance, blood pressure and cardiac output remained unaltered. Acetaminophen rate of appearance was similar between groups (\n                      <jats:italic>P<\/jats:italic>\n                      =0.707), indicating comparable nutrient absorption rates. POTS had increased plasma levels of C-peptide (\n                      <jats:italic>P<\/jats:italic>\n                      =0.001), GIP (glucose-dependent insulinotropic polypeptide;\n                      <jats:italic>P<\/jats:italic>\n                      =0.001), peptide YY (\n                      <jats:italic>P<\/jats:italic>\n                      =0.016), and pancreatic polypeptide (\n                      <jats:italic>P<\/jats:italic>\n                      =0.04) following glucose consumption, but only GIP had a time-dependent association with the worsening upright tachycardia and stroke volume fall.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>The glucose-induced worsening orthostatic tachycardia in POTS was associated with a decline in SV; these changes occurred while GIP, a splanchnic vasodilator, was maximally elevated.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/hypertensionaha.121.17852","type":"journal-article","created":{"date-parts":[[2022,3,2]],"date-time":"2022-03-02T05:00:12Z","timestamp":1646197212000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":17,"title":["Worsening Postural Tachycardia Syndrome Is Associated With Increased Glucose-Dependent Insulinotropic Polypeptide Secretion"],"prefix":"10.1161","volume":"79","author":[{"given":"Nicholas C.","family":"Breier","sequence":"first","affiliation":[{"name":"Department of Medicine, Division of Clinical Pharmacology (N.C.B., S.Y.P., S.S., S.E.M., A.D., L.E.O., C.A.S.), Vanderbilt University Medical Center, Nashville, TN."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sachin Y.","family":"Paranjape","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Clinical Pharmacology (N.C.B., S.Y.P., S.S., S.E.M., A.D., L.E.O., C.A.S.), Vanderbilt University Medical Center, Nashville, TN."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shea","family":"Scudder","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Clinical Pharmacology (N.C.B., S.Y.P., S.S., S.E.M., A.D., L.E.O., C.A.S.), Vanderbilt University Medical Center, Nashville, TN."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shahram E.","family":"Mehr","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Clinical Pharmacology (N.C.B., S.Y.P., S.S., S.E.M., A.D., L.E.O., C.A.S.), Vanderbilt University Medical Center, Nashville, TN."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andre\u2019","family":"Diedrich","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Clinical Pharmacology (N.C.B., S.Y.P., S.S., S.E.M., A.D., L.E.O., C.A.S.), Vanderbilt University Medical Center, Nashville, TN."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charles R.","family":"Flynn","sequence":"additional","affiliation":[{"name":"Department of Surgery (C.R.F.), Vanderbilt University Medical Center, Nashville, TN."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6914-7287","authenticated-orcid":true,"given":"Luis E.","family":"Okamoto","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Clinical Pharmacology (N.C.B., S.Y.P., S.S., S.E.M., A.D., L.E.O., C.A.S.), Vanderbilt University Medical Center, Nashville, TN."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bolette","family":"Hartmann","sequence":"additional","affiliation":[{"name":"Novo Nordisk Foundation Center for Basic Metabolic Research (B.H.), University of Copenhagen, Denmark."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7880-8515","authenticated-orcid":true,"given":"L\u00e6rke Smidt","family":"Gasbjerg","sequence":"additional","affiliation":[{"name":"Department of Biomedical Science (B.H., L.S.G.), University of Copenhagen, Denmark."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4518-6801","authenticated-orcid":true,"given":"Cyndya A.","family":"Shibao","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Clinical Pharmacology (N.C.B., S.Y.P., S.S., S.E.M., A.D., L.E.O., C.A.S.), Vanderbilt University Medical Center, Nashville, TN."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_3_2_2","unstructured":"Collins FS. 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