Utility of Growth Hormone and Other Potential Agents to Restore Enteral Autonomy in Short Bowel Syndrome
John K. DiBaise, Carol Rees Parrish, Jon S. Thompson in Short Bowel Syndrome Practical Approach to Management, 2017
Peptide YY, also produced by L-cells in the distal small bowel and proximal colon, is an important motility-modulating hormone that, because of its effects to slow gastrointestinal transit (mediator of the ileal and colonic brakes), might play a role in facilitating fluid and nutrient absorption. As might be expected, its levels are diminished in patients without ileum or colon, but levels are markedly elevated in SBS patients with a colon remaining [58]. Furthermore, despite earlier reports not identifying intestinotrophic properties of peptide YY, a recent report found that peptide YY induces intestinal proliferation in peptide YY knockout mice also receiving total EN after massive small bowel resection [59]. Although a peptide YY analog is available, to our knowledge, it has yet to be studied in humans with SBS.
Obesity
Mary J. Marian, Gerard E. Mullin in Integrating Nutrition Into Practice, 2017
Another hormone, which plays a role in the delay of gastric emptying and reduction of gastric secretion, is peptide YY (PYY). PYY is released after meal ingestion and signals to the hypothalamus. It is found throughout the intestine at progressively higher levels distally, with the highest levels in the colon and the rectum. It is secreted by the L cells of the distal small bowel and colon. Administration of PYY before meals results in decreased food consumption [40]. Cholecystokinin (CCK), which is produced in the gallbladder, pancreas, and stomach, and concentrated in the small intestine, also controls gastric emptying and gut motility. CCK acts centrally by increasing satiety and decreasing appetite [41]. Glucagon-like peptide-1 enhances satiety and reduces food intake when administered intravenously to humans [42]. It is a potent regulator of food intake in humans.
Humoral Factors in Nausea and Emesis
John Kucharczyk, David J. Stewart, Alan D. Miller in Nausea and Vomiting: Recent Research and Clinical Advances, 2017
Emesis has been reported in dogs following i.v. bolus injection of a chromatographic subfraction derived from porcine small intestinal extracts.79 The active principle has been shown to be the 36 amino acid peptide YY (PYY). The threshold for an i.v. bolus injection into dogs of synthetic PYY was 120 pmol/kg and the ED50 in a large population was 325 pmol/kg. The related peptides, pancreatic polypeptide (PP) and neuropeptide Y (NPY), were either much less effective emetics (NPY) or ineffective (PP). In the ferret, another animal which, like the dog, exhibits a highly sensitive emetic reflex, PYY (3 μg/kg) was an effective i.v. emetic in 36% of the animals tested.102 These results show that PYY is the most potent circulating emetic peptide identified to date.
Relationship Between Appetite-Related Peptides and Frailty in Older Adults
Published in Endocrine Research, 2023
Burcu Candemir, İbrahim İleri, Mehmet Muhittin Yalçın, Aydın Tuncer Sel, Berna Göker, Özlem Gülbahar, İlhan Yetkin
Peptide YY is a peptide that is secreted from the ileum and colon in response to nutrition and reduces appetite and hence called “ileal brake.” It inhibits the secretion of ghrelin, delays gastric emptying, and suppresses the secretory function of the pancreas and stomach.30 It also works centrally by inhibiting mRNA expression of NPY and AgRP in the arcuate nucleus.30 Alpha MSH, which is the product of the POMC gene, has a significant impact on food intake and energy balance. The effects of α-MSH on food intake and body weight are mediated in the brain via two melanocortin receptors (MCR), MC3-R and MC4-R. Melanocortin receptor-4 is localized primarily in the central nervous system and is responsible for the appetite-reducing effects of α -MSH. Functional mutations of MC4-R have been associated with hyperphagia and obesity in mice.31 CART is an anorexigenic hormone that shows its anorexigenic effect through the inhibition of NPY neurons and central release of glucagon-like peptide-1.32 Some authors reported increased CART mRNA expression with aging, while others found no changes.33–35 In the present study, our results suggested that α-MSH and CART levels were independent predictors of frailty. However, small predictive values raise the question of whether our findings are of any possible clinical significance. Nevertheless, the results of this study, which have a novel premise, will shed light on future studies.
Novel approaches to anti-obesity drug discovery with gut hormones over the past 10 years
Published in Expert Opinion on Drug Discovery, 2019
Frances Rose, Stephen Bloom, Tricia Tan
Peptide YY (PYY) is a hormone belonging to the pancreatic polypeptide (PP) family, and is secreted by the neuroendocrine L-cells of the small intestine in response to eating [28]. Its effect is mediated through the neuropeptide Y (NPY) receptors, of which there are several subtypes. The hypothalamic arcuate nucleus, which is a key area in central appetite regulation, expresses the Y2 receptor (Y2R). PYY3–36 is derived from full length PYY1–36 by dipeptidyl peptidase-IV (DPP-IV), and is more selective for Y2R. Plasma PYY3–36 levels rise within 15 minutes of ingesting food, with peak levels proportional to the number of calories ingested [29]. Administration of PYY by infusion in humans leads to reduced food intake, an effect which is preserved in obesity. Obese subjects have also been shown to have lower endogenous levels of PYY, therefore making it a potential therapeutic target for appetite suppression [30].
Obesity medications in development
Published in Expert Opinion on Investigational Drugs, 2020
Candida J. Rebello, Frank L. Greenway
Peptide YY (PYY) which is released post-prandially is a well-characterized mediator of satiety and exerts its effects through the Y family of receptors. It is released from the L cells of the GI tract throughout the gut but is present in the highest concentrations in the distal regions. The most effective form is the amino-terminally truncated version, PYY3-36, since the full form binds with little affinity to the Y receptors [16]. The preferred Y2 receptor is highly expressed in orexigenic neuropeptide Y neurons in the hypothalamic arcuate nucleus. Peripheral administration of PYY3-36 reduces food intake in rodents and humans [17,18]. The results in rodents could not be replicated [19] and in humans the anorectic effect was evident only at pharmacologic doses [20].
Related Knowledge Centers
- Anorectic
- Chyme
- Dietary Fiber
- Ileum
- Pancreatic Polypeptide
- Amino Acid
- Large Intestine
- Gene
- Neuropeptide Y Receptor Y2
- Neuropeptide Y Receptor