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The Small IntestineSecretions, Digestion and Motility
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Pancreatic polypeptide is released from the pancreas by all three food types, the most important being a protein meal. It inhibits both pancreatic enzyme and secretion. Peptide YY is synthesized and released by enteroendocrine cells in the jejunum in response to fat. It has mainly inhibitory actions; inhibiting gastric motility and secretion as well as chloride secretion by intestinal epithelium.
Physical Activity in the Prevention of Obesity
Published in Roy J. Shephard, Obesity: A Kinesiologist’s Perspective, 2018
Some investigators have approached the issue from the viewpoint of possible changes in the secretion of hormones regulating appetite. In a number of reports, bouts of moderate to vigorous running have had little impact upon circulating levels of the appetite-suppressing hormone ghrelin [21, 52, 60, 111]. A handful of recent studies have added that although vigorous exercise induces a transient reduction in the production of acylated ghrelin, it does not change circulating levels of ghrelin independently of weight loss. Moreover, exercise increases levels of peptide YY, a hormone that suppresses appetite [55].
Medical complications of eating disorders
Published in Stephen Wonderlich, James E Mitchell, Martina de Zwaan, Howard Steiger, Eric F van Furth, Annual Review of Eating Disorders Part 1 – 2007, 2018
Increasingly, neuropeptides and hormones have been shown to play an important role in the regulation of appetite and body weight. Three have received much attention in eating disorder patients: leptin, peptide YY, and ghrelin. Recent reviews of leptin functioning have identified abnormalities in leptin physiology in both AN and BN, and its potential role in their treatment (Monteleone et al. 2004; Chan and Mantzoros 2005). The exact role these disturbances play in the etiology or maintenance of these disorders remains to be elucidated. A recent study found elevated peptide YY levels in AN subjects (Misra et al. 2006). These elevated levels may contribute to reduced intake and decreased bone turnover in AN. Abnormalities in ghrelin secretion have recently been reported in AN and obesity (Gottero et al. 2004).
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.
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].
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].