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Am J Physiol Regul Integr Comp Physiol 278: R1217-R1223, 2000;
0363-6119/00 $5.00
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Vol. 278, Issue 5, R1217-R1223, May 2000

Relationship between increasing duodenal lipid doses, gastric perception, and plasma hormone levels in humans

Christine Feinle1, David Grundy2, Bärbel Otto3, and Michael Fried1

1 Gastroenterology Division, University Hospital Zurich, CH-8091 Zurich, Switzerland; 2 Department of Biomedical Sciences, University of Sheffield, S102TN United Kingdom; and 3 Medizinische Klinik, Klinikum Innenstadt, University of Munich, D-80366 Munich, Germany

Duodenal lipid causes gastric relaxation, CCK secretion, and nausea. Vasopressin has been implicated in motion sickness-related nausea. We hypothesized that increasing doses of lipid enhance gastric relaxation and CCK-vasopressin secretion, resulting in a dose-related exacerbation of nausea. Nine healthy subjects received isotonic saline or lipid (1, 2, or 3 kcal/min, L1, L2, L3) duodenally. Changes in gastric volume, sensations, and plasma hormone levels were assessed during infusions and isobaric gastric distensions. Lipid infusions increased gastric volume, plasma CCK (but not vasopressin) levels, and gastric compliance during distensions, compared with saline. Plasma CCK levels were related to the dose of lipid administered [CCK levels at 30 min (pmol/l), saline: 1.1 ± 0.2, L1: 1.8 ± 0.2, L2: 3.0 ± 0.2, L3: 4.3 ± 0.6]. During distensions, nausea increased in intensity with increasing doses of lipid [score (where 0 is no sensation and 100 is strongest sensation), saline: 7 ± 4, L1: 19 ± 7, L2: 44 ± 7, L3: 66 ± 8]; however, no further rise in plasma CCK occurred. Because neither lipid nor distension alone induced significant nausea, we conclude that the interaction between these stimuli together with a modulation by CCK is responsible for the effects observed. Vasopressin is not involved in lipid- and distension-induced nausea.

cholecystokinin; gastric distension; nausea; vasopressin; dose-response relationship


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