PYY and GLP-1 contribute to feedback inhibition from the canine ileum and colon

Wen, Jipu; Phillips, Sidney F.; Sarr, Michael G.; Kost, Louis J.; Holst, JJ

doi:10.1152/ajpgi.1995.269.6.g945

Cited by 79 publications

(52 citation statements)

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“…The ability of PYY(3-36) to inhibit gastric emptying is consistent with the suggested role of PYY and its derivatives in the ileal brake (14,22,25). In the present study, PYY(3-36) induced a dose-related suppression of liquid gastric emptying that was maximal at a dose of 3 nmol/kg.…”

Section: Discussionsupporting

confidence: 90%

Peptide YY(3–36) inhibits gastric emptying and produces acute reductions in food intake in rhesus monkeys

Moran

Smedh

Kinzig

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

161

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inhibits gastric emptying and produces acute reductions in food intake in rhesus monkeys. Am J Physiol Regul Integr Comp Physiol 288: R384 -R388, 2005. First published September 23, 2004 doi:10.1152/ ajpregu.00535.2004], a gastrointestinal peptide that is released into the circulation in response to ingesting a meal, has recently been suggested to play a role in controlling food intake. PYY(3-36) has been reported to inhibit food intake following peripheral administration in rodents and in human subjects. To more fully characterize the potential feeding actions of PYY(3-36), we examined the ability of a dose range of PYY(3-36) (0.3-3.0 nmol/kg) to affect liquid gastric emptying and daily 6-h food intake in male rhesus monkeys. Intramuscular PYY(3-36) produced a dose-related inhibition of saline gastric emptying that was maximal at a dose of 3 nmol/kg. Intramuscular PYY(3-36) administered before daily 6-h food access produced significant feeding reductions at doses of 1 and 3 nmol/kg. Analyses of the patterns of food intake across the 6-h period of food access revealed that PYY(3-36) increased the latency to the first meal and reduced average meal size without altering meal number. Although single doses of PYY(3-36) reduced intake, a suppressive effect on food intake was not sustained over multiple administrations across successive days. Together, these data suggest that PYY(3-36) has the ability to reduce food intake in acute test situations in nonhuman primates. Whether this is a physiological action of the endogenous peptide remains to be determined. satiety; meal patterns; gut peptides CONSUMED NUTRIENTS EXCITE the release of a variety of gastrointestinal peptides that serve as feedback signals for coordinating nutrient movement through the gastrointestinal tract, absorption, and metabolism. Different peptides have different sites and patterns of release. Roles for some of those peptides in the controls of food intake have been proposed and/or documented.Recently, peptide YY 3-36 ] has been demonstrated to reduce food intake in rodents and humans. Batterham and colleagues (4) reported significant suppression of food intake in mice and rats in response to peripheral bolus PYY(3-36) administration and significant decreases in food intake in human subjects in response to infusions. An action of peripheral PYY(3-36) through arcuate nucleus Y2 receptors was proposed. The Y2 receptor is a presynaptic inhibitory receptor, and PYY(3-36) has been demonstrated to have relative specificity for this neuropeptide Y (NPY) receptor subtype (13). Consistent with this proposal, PYY(3-36) was shown to inhibit food intake when injected into the arcuate nucleus in intact, but not in Y2 Ϫ/Ϫ , mice, and PYY(3-36) increased activity in proopiomelanocortin (POMC) neurons through decreasing the frequency of inhibitory postsynaptic currents, indicative of a decrease in GABA release. Because arcuate NPY neurons exert a tonic GABAergic inhibitory influence on arcuate POMC neurons, this action of PYY(3-36) was interpreted to support ...

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Section: Discussionsupporting

confidence: 90%

Peptide YY(3–36) inhibits gastric emptying and produces acute reductions in food intake in rhesus monkeys

Moran

Smedh

Kinzig

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

161

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“…NT, GLP-1 and PYY have all been implicated as mediating the ileal brake re¯ex on upper gut motility when nutrients are infused into the ileum. 6,26 In the light of this, and the elevated levels of gut hormones shown in this study, one would expect to ®nd a slower rate of gastric emptying in the obese subjects operated with JIB 20 years ago than in non-operated obese controls.…”

Section: Discussionmentioning

confidence: 76%

Gastrointestinal hormones and gastric emptying 20 years after jejunoileal bypass for massive obesity

et al. 1997

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OBJECTIVE: Some studies have shown a more rapid gastric emptying in obese subjects. Six to twelve months after jejunoileal bypass (JIB) neurotensin (NT) and enteroglucagon have been shown to be elevated after food intake. These hormones, together with peptide YY (PYY) and glucagon-like peptide-1 (GLP-1) have been implicated in the reduction of upper gastrointestinal motility seen after infusion of nutrients into the ileum. AIM: To study if the postprandial gut hormone pattern and gastric emptying is altered 20 y after JIB. SUBJECTS: Seven subjects operated with JIB a mean (s.d.) 20 AE 3 y ago, with a BMI of 44 AE 4 kg/m 2 at the time of surgery and 31 AE 4 at present. For comparison seven sex-matched non-operated obese controls (BMI 43 AE 3) were studied. METHODS: Serial blood samples were obtained every 10 min after intake of a 280 kcal meal. Radioimmunoassays for motilin, cholecystokinin (CCK), NT, PYY and GLP-1 were performed. Gastric emptying of a solid meal was studied using a radioactively labelled omelette (of 310 kcal) for 120 min). RESULTS: After JIB postprandial motilin, CCK, NT, PYY and GLP-1 were elevated compared to non-operated obese subjects. Similarly, basal levels of CCK, motilin, GLP-1 and PYY were elevated in the operated group. No difference was observed in the rate of gastric emptying between the two groups. CONCLUSION: Both fasting and postprandial gut hormone levels are elevated 20 y after JIB. The impact of long-term rapid stimulation of the ileum and subsequent raised gut hormone levels on gastric emptying is not clear.

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“…Additionally, PYY and NT were released. In contrast, plasma PYY levels were elevated by ileal perfusion of casein hydrolysate in dogs, whereas plasma NT concentrations were not modified (24). In humans, another study showed that plasma levels of PYY and GLP-1 were not altered after ileal perfusion with peptone (9).…”

Section: Discussionmentioning

confidence: 99%

Peptide YY, Glucagon-Like Peptide-1, and Neurotensin Responses to Luminal Factors in the Isolated Vascularly Perfused Rat Ileum

et al. 1998

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Exposure of the ileum to nutrients markedly inhibits several upper gastrointestinal functions. Hormonal peptides of the ileal wall, i.e. peptide YY (PYY), glucagon-like peptide-1 (GLP-1), and neurotensin (NT), are thought to play a role in this negative feedback mechanism. The present study was conducted to comparatively assess the secretion of PYY, GLP-1, and NT upon luminal infusion of a variety of individual luminal factors in the isolated vascularly perfused rat ileum preparation. PYY, GLP-1, and NT were measured in the portal effluent with specific RIAs. Glucose (250 mM) induced a pronounced release of the three peptides, whereas a physiological concentration of 5 mM did not induce peptide secretion. Peptone (5%, wt/vol) evoked a sustained release of PYY, GLP-1, and NT. Only NT secretion was increased upon luminal administration of 100 mM sodium oleate.Short chain fatty acids (20 mM) evoked an early and transient release of the three peptides. In contrast, taurocholate (20 mM) induced a sustained release of PYY, GLP-1, and NT, but the threshold concentration for peptide release was lower for NT than for PYY or GLP-1. Cellulose or pectin (0.5%, wt/vol) did not modify peptide secretion. In conclusion, glucose and peptone are potent stimulants of PYY, GLP-1, and NT release. Only NT is released upon oleic acid stimulation. Finally, taurocholate is a potent stimulant of the release of the three peptides. Overall, PYY, GLP-1, and NT may participate cooperatively in the ileal brake. As relatively high concentrations of the various stimulants were required to elicit peptide release, it seems likely that this mechanism operates in cases of maldigestion or malabsorption. (Endocrinology 139: 3780 -3786, 1998) U NABSORBED nutrients reaching the ileum influence the functions of the upper gut to increase the efficiency of digestion and absorption. For example, unabsorbed fat or protein in the ileum delays the passage of material through the small intestine. As a delay in small bowel transit increases the contact time between luminal contents and absorptive epithelium, this mechanism may serve to increase the absorption of a meal. This negative feedback mechanism referred to as the ileal brake presumably involves hormonal intermediates. As the ileal mucosa contains several distinct populations of endocrine cells, many studies focused on the effects of the products of these cells on gastrointestinal functions. Neurotensin (NT), the major product of the so-called N cells, and peptide YY (PYY) and glucagon-like peptide 1 (GLP-1), which are cosynthesized in the so-called L cells, have been implicated in these feedback mechanisms.Circulating levels of NT, PYY, and GLP-1 rapidly increase in response to oral ingestion of a mixed meal, thus suggesting that their release is triggered in part by hormonal and/or neural signals originating from the upper small intestine. As NT, PYY, and GLP-1 are contained in open-type cells, nutrients making contact with the ileal mucosa are also capable of eliciting peptide secretion. In...

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PYY and GLP-1 contribute to feedback inhibition from the canine ileum and colon

Cited by 79 publications

References 0 publications

Peptide YY(3–36) inhibits gastric emptying and produces acute reductions in food intake in rhesus monkeys

Peptide YY(3–36) inhibits gastric emptying and produces acute reductions in food intake in rhesus monkeys

Gastrointestinal hormones and gastric emptying 20 years after jejunoileal bypass for massive obesity

Peptide YY, Glucagon-Like Peptide-1, and Neurotensin Responses to Luminal Factors in the Isolated Vascularly Perfused Rat Ileum

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