Ileal brake: Neuropeptidergic control of intestinal transit

Abstract

Digestion and absorption of a meal are time-intensive processes. To optimize digestion and absorption, transit of the meal through the gastrointestinal tract is regulated by a complex integration of neuropeptidergic signals generated as the jejunal brake and ileal brake response to nutrients. Mediators involved in the slowing of transit responses include peptide YY (PYY), chemosensitive afferent neurons, intestinofugal nerves, noradrenergic nerves, myenteric serotonergic neurons, and opioid neurons. The activation of this circuitry modifies the peristaltic reflex to convert the intestinal motility pattern from propagative to segmenting. Fat is the most potent trigger of these transit control mechanisms. The integrated circuitry of gut peptides and neurons involved in transit control in response to nutrients is described in this review.

Absorption, metabolism, and excretion of green tea flavan‐3‐ols in humans with an ileostomy

“…The ileostomists had earlier T max values than subjects with colon, for all the absorbed flavan-3-ols and their metabolites (Table 5). This is probably due to more rapid transit through the small intestine due to the absence of an ileal brake [28,29]. Once absorbed into the circulatory system, the various flavan-3-ols appeared to behave in a similar manner as the presence or absence of a colon did not impact on plasma T 1/2 values ( Table 5).…”

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

“…9,10,38 PYY is released from L-endocrine cells of which the high concentrations in humans are found in the distal small intestine, colon and rectum, with progressively more PYY-producing cells when going distally in the gut. The most powerful stimulants for PYY release is fat, especially (triglycerides consisting of) long-chain fatty acids, although amino acids and even carbohydrates have been shown to be effective.…”

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.…”