Effects of fat digestion on appetite, APD motility, and gut hormones in response to duodenal fat infusion in humans

Abstract

The presence of nutrients in the small intestine slows gastric emptying and suppresses appetite and food intake; these effects are partly mediated by the release of gut hormones, including CCK. We investigated the hypothesis that the modulation of antropyloroduodenal motility, suppression of appetite, and stimulation of CCK and glucagon-like peptide-1 secretion by intraduodenal fat are dependent on triglyceride hydrolysis by lipase. Sixteen healthy, young, lean men were studied twice in double-blind, randomized, crossover fashion. Ratings for appetite-related sensations, antropyloroduodenal motility, and plasma CCK and glucagon-like peptide-1 concentrations were measured during a 120-min duodenal infusion of a triglyceride emulsion (2.8 kcal/min) on one day with, on the other day without, 120 mg tetrahydrolipstatin, a potent lipase inhibitor. Immediately after the duodenal fat infusion, food intake at a buffet lunch was quantified. Lipase inhibition with tetrahydrolipstatin was associated with reductions in tonic and phasic pyloric pressures, increased numbers of isolated antral and duodenal pressure waves, and stimulation of antropyloroduodenal pressure-wave sequences (all P < 0.05). Scores for prospective consumption and food intake at lunch were greater, and nausea scores were slightly less, and the rises in plasma CCK and glucagon-like peptide-1 were abolished (all P < 0.05). In conclusion, lipase inhibition attenuates the effects of duodenal fat on antropyloroduodenal motility, appetite, and CCK and glucagon-like peptide-1 secretion.

Dose-related effects of lauric acid on antropyloroduodenal motility, gastrointestinal hormone release, appetite, and energy intake in healthy men

“…For example, infusion of C12 at doses as low as 0.1 and 0.2 kcal/min, resulting in a total energy delivery of only 9 and 14 kcal, respectively, over the 90-min infusion period, had substantial effects. In previous studies using intraduodenal lipid infusion at a rate of 2.8 kcal/min, the stimulation of pyloric motility and plasma CCK concentrations were maximal at ϳ30 -45 min, when ϳ84 -126 kcal would have been delivered to the small intestine (10). This contrasts with the current study in which maximal effects of C12 infusion on pyloric motility and plasma hormone secretion were observed after 15 min, when only 1.5, 3, or 6 kcal had been delivered to the small intestine during infusion of C12 at 0.1, 0.2, or 0.4 kcal/min, respectively.…”

“…In conclusion, intraduodenal C12 dose-dependently modulated APD motility and gastrointestinal hormone release in healthy male subjects, whereas effects on energy intake were only apparent with the highest dose infused (0.4 kcal/min), possibly because only at this dose was modulation of APD motility and gastrointestinal hormone secretion sufficient for a suppressant effect on energy intake. free fatty acid; cholecystokinin; glucagon-like peptide-1; pyloric motility STUDIES UTILIZING PHARMACOLOGICAL AGENTS, such as tetrahydrolipstatin, to inhibit fat digestion have provided evidence that the effects of fat on gastric emptying, gastrointestinal motility, gastrointestinal hormone secretion, and appetite are dependent on the presence of free fatty acids in the small intestine (4,10,11,22,27,29,33). The effects of free fatty acids on gastrointestinal function, including motility, hormone release, and energy intake (12,16,22,23), also are dependent on their acyl chain length.…”

Effect of ileal fat perfusion on satiety and hormone release in healthy volunteers

“…First, triacylglycerols need to be hydrolyzed to fatty acids to be able to reduce satiety and food intake. 25 It is well known that the lipolytic capacity in the ileum is smaller compared with the duodenum. 26 A lack of lipase in the ileum may have limited the hydrolysis of the high fat dose.…”

No appetite efficacy of a commercial structured lipid emulsion in minimally processed drinks

“…This is a satiety response stimulated by the presence of slowly digested nutrients (fat in this case) in the distal small intestine, 5,23 and involves an increase in the release of the satiety hormone GLP-1. 1 --4 Not just GLP-1, but also CCK, 24 PYY 25 and the opioid system 26 have been implicated in the ileal brake mechanism. Amounts of fat as a low as 3 g delivered directly to the ileum have been shown to trigger this mechanism, 26 suggesting that such effects of a structured food emulsion are at least plausible.…”