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

Abstract

Objective: The ileal brake is a feedback mechanism activated by nutrients, especially fat, with marked effects on satiety. The effects of low doses of ileal fat on satiety are largely unknown. We therefore studied the effect of ileal vs oral delivery of low doses of fat on satiety and gut peptide secretion. Design: Randomized, single-blind crossover design. Subjects: Sixteen healthy, normal-weight volunteers (6 male; mean age 26 years, mean body mass index 22.4). Intervention: Participants were intubated with a 290-cm-long nasoileal tube and consumed, on 3 consecutive days, either a liquid breakfast with 3 g fat followed by an ileal placebo infusion at t ¼ 105-150 min (treatment C) or a fat-free liquid breakfast followed by an ileal infusion of either an emulsion of 3 g (treatment I3g) or 9 g (treatment I9g) fat (safflower oil). Measurements: Satiety parameters by visual analog scales and plasma concentrations of CCK and PYY. Results: C significantly increased satiety and CCK secretion compared with the fat-free breakfast. Ileal fat perfusion of both 3 and 9 g (I3g and I9g) significantly increased satiety during and after fat perfusion, without differences in satiety between I3g and I9g. During ileal fat infusion, CCK increased dose dependently, whereas PYY concentrations increased significantly only after 9 g of fat. Secretion of CCK but not of PYY correlated to satiety levels. Conclusion: Postprandial satiety following a liquid breakfast can be effectively and significantly increased by small amounts (as little as 3 g) of fat perfused into the ileum. Ileal fat dose-dependently increased CCK but not PYY secretion. The satiating effect of ileal fat may be partly mediated by CCK.

Diet and Irritable Bowel Syndrome, with a Focus on Appetite-Regulating Gut Hormones

“…Circulating PYY 3-36 binds to Y2 receptors on the presynaptic terminals of hypothalamic neuropeptide Y (NPY) and agouti-related protein (AgRP) neurons, and inactivation of these neurons is associated with the induction of anorexia [186]. PYY is a major regulator of the ileal brake in that it acts to inhibit further food intake once nutrients, and especially lipids, have reached the distal small intestine (ileum) [187][188][189][190][191][192][193][194][195][196]. The density of PYY cells is generally decreased in sporadic IBS (Table 1.1 and Fig.…”

Biophysical Aspects of Lipid Digestion in Human Breast Milk and Similac™ Infant Formulas

“…[42][43][44] Bile salts not only facilitate the adsorption of co-lipase and lipase, but also aid in the solubilization of the lipolysis products as they accumulate at the interface, into mixed micelles, allowing the transport to and through the gut mucosal surface [28]. The gut cell lining is then able to sense these nutrients and in response, secrete hormones and peptides that slow digestion and send signals to the brain that reduce appetite [45].…”

The multifactorial interplay of diet, the microbiome and appetite control: current knowledge and future challenges

“…Landmark human studies have shown intestinal nutrient infusions can reduce food intake with rapid effects (48)(49)(50) , indicating that satiation signals must originate from the gut as well as post-absorptively. Numerous hormones, neurotransmitters and peptides stimulate orexigenic or anorexigenic responses.…”