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

Duodenal lipid causes gastric relaxation, CCK secretion, and nausea. Vasopr essin has been implicated in motion sickness-related nausea. We hypothesize d that increasing doses of lipid enhance gastric relaxation and CCK-vasopre ssin secretion, resulting in a dose-related exacerbation of nausea. Nine he althy subjects received isotonic saline or lipid (1, 2, or 3 kcal/min, L1, L2, L3) duodenally. Changes in gastric volume, sensations, and plasma hormo ne 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. Pl asma 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 in creasing doses of lipid [score (where 0 is no sensation and 100 is stronges t sensation), saline: 7 +/- 4, L1: 19 +/- 7, L2: 44 +/- 7, L3: 66 +/- 8]; h owever, no further rise in plasma CCK occurred. Because neither lipid nor d istension alone induced significant nausea, we conclude that the interactio n between these stimuli together with a modulation by CCK is responsible fo r the effects observed. Vasopressin is not involved in lipid- and distensio n-induced nausea.