Fat digestion modulates gastrointestinal sensations induced by gastric distention and duodenal lipid in humans.
OBJECTIVE
It is unclear whether fat digestion is required for the induction of gastrointestinal sensations and whether different fats have different effects. We investigated the effect of fat digestion and of medium-chain triglycerides (MCTs; C < 12) and long-chain triglycerides (LCTs; C > 16) on gastrointestinal sensations.


METHODS
In a double-blind study, 15 healthy subjects were studied on 5 occasions during which LCT or MCT emulsions (2 kcal/min), with or without 120 mg tetrahydrolipstatin (THL, lipase inhibitor), or sucrose polyester (SPE, nondigestible fat) were infused intraduodenally in randomized order. After 30 minutes, the proximal stomach was distended in 1 mm Hg steps/min. Intensity of gastrointestinal sensations (on a 0-10 visual analog scale), plasma cholecystokinin (CCK) levels, and gastric volumes were assessed throughout.


RESULTS
LCT and MCT increased gastric volume at baseline pressure compared with SPE, and LCT more than MCT. THL entirely abolished this effect (volumes [mL]: LCT, 213 +/- 19; LCT-THL, 39 +/- 3; MCT, 155 +/- 12; MCT-THL, 43 +/- 5; SPE, 44 +/- 5). Only LCT increased plasma CCK levels (pmol/L per 30 minutes: LCT, 21 +/- 2; LCT-THL, 9 +/- 1; MCT, 9 +/- 1; MCT-THL, 11 +/- 1; SPE, 9 +/- 1). During distentions, intragastric volumes were greater during infusion of LCT and MCT than during the respective THL conditions or SPE, but plasma CCK levels did not change. The intensity of sensations increased (hunger decreased) more with LCT than with MCT. During infusion of THL or SPE, the effects were smaller than during LCT or MCT.


CONCLUSIONS
Fat digestion is required for the modulation of gastrointestinal sensations during gastric distention. The effects of fat depend on the fatty acid chain length and are not entirely explained by release of CCK.
Feinle
C
C
Gastroenterology Division, University Hospital Zurich, Switzerland.
Rades
T
T
Otto
B
B
Fried
M
M
D000328:Adult; D002766:Cholecystokinin / Q000097:blood; D004041:Dietary Fats / Q000493:pharmacokinetics*; D004063:Digestion / Q000502:physiology; D004386:Duodenum / Q000294:innervation / Q000378:metabolism*; D004750:Enteral Nutrition; D004791:Enzyme Inhibitors / Q000008:administration & dosage; D019358:Fat Substitutes / Q000493:pharmacokinetics; D005227:Fatty Acids / Q000493:pharmacokinetics; D005230:Fatty Acids, Nonesterified / Q000493:pharmacokinetics; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism*; D006801:Humans; D006815:Hunger / Q000502:physiology; D007783:Lactones / Q000008:administration & dosage; D008049:Lipase / Q000037:antagonists & inhibitors; D008297:Male; D000077403:Orlistat; D011312:Pressure; D012677:Sensation / Q000187:drug effects* / Q000502:physiology; D013270:Stomach / Q000294:innervation; D013395:Sucrose / Q000031:analogs & derivatives* / Q000493:pharmacokinetics; D014280:Triglycerides / Q000493:pharmacokinetics
D004041:Dietary Fats; D004791:Enzyme Inhibitors; D019358:Fat Substitutes; D005227:Fatty Acids; D005230:Fatty Acids, Nonesterified; D007783:Lactones; D014280:Triglycerides; D013395:Sucrose; C013692:sucrose polyester; D002766:Cholecystokinin; D000077403:Orlistat; D008049:Lipase