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1.
Possible role of peptide YY (PYY) in the pathophysiology of irritable bowel syndrome (IBS).
El-Salhy, M, Hatlebakk, JG, Hausken, T
Neuropeptides. 2020;:101973
Abstract
Irritable bowel syndrome (IBS) is a common gastrointestinal disorder of unknown aetiology for which there is no effective treatment. Although IBS does not increase mortality, it reduces the quality of life and is an economic burden to both the patients themselves and society as a whole. Peptide YY (PYY) is localized in endocrine cells located in the ileum, colon and rectum. The concentration of PYY and the density of PYY cells are decreased in both the colon and rectum but unchanged in the ileum of patients with IBS. The low density of PYY cells in the large intestine may be caused by a decreased number of stem cells and their progeny toward endocrine cells. PYY regulates the intestinal motility, secretion and absorption as well as visceral sensitivity via modulating serotonin release. An abnormality in PYY may therefore contribute to the intestinal dysmotility and visceral hypersensitivity seen in IBS patients. Diet management involving consuming a low-FODMAP diet restores the density of PYY cells in the large intestine and improves abdominal symptoms in patients with IBS. This review shows that diet management appears to be a valuable tool for correcting the PYY abnormalities in the large intestine of IBS patients in the clinic.
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2.
Ghrelin, CCK, GLP-1, and PYY(3-36): Secretory Controls and Physiological Roles in Eating and Glycemia in Health, Obesity, and After RYGB.
Steinert, RE, Feinle-Bisset, C, Asarian, L, Horowitz, M, Beglinger, C, Geary, N
Physiological reviews. 2017;(1):411-463
Abstract
The efficacy of Roux-en-Y gastric-bypass (RYGB) and other bariatric surgeries in the management of obesity and type 2 diabetes mellitus and novel developments in gastrointestinal (GI) endocrinology have renewed interest in the roles of GI hormones in the control of eating, meal-related glycemia, and obesity. Here we review the nutrient-sensing mechanisms that control the secretion of four of these hormones, ghrelin, cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), and peptide tyrosine tyrosine [PYY(3-36)], and their contributions to the controls of GI motor function, food intake, and meal-related increases in glycemia in healthy-weight and obese persons, as well as in RYGB patients. Their physiological roles as classical endocrine and as locally acting signals are discussed. Gastric emptying, the detection of specific digestive products by small intestinal enteroendocrine cells, and synergistic interactions among different GI loci all contribute to the secretion of ghrelin, CCK, GLP-1, and PYY(3-36). While CCK has been fully established as an endogenous endocrine control of eating in healthy-weight persons, the roles of all four hormones in eating in obese persons and following RYGB are uncertain. Similarly, only GLP-1 clearly contributes to the endocrine control of meal-related glycemia. It is likely that local signaling is involved in these hormones' actions, but methods to determine the physiological status of local signaling effects are lacking. Further research and fresh approaches are required to better understand ghrelin, CCK, GLP-1, and PYY(3-36) physiology; their roles in obesity and bariatric surgery; and their therapeutic potentials.
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3.
Appetite-related peptides in childhood and adolescence: role of ghrelin, PYY, and GLP-1.
Horner, K, Lee, S
Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme. 2015;(11):1089-99
Abstract
During childhood and adolescence, a number of factors, including age, puberty, sex, race, and body composition, may contribute to differences in satiety, food intake, and appetite-related peptides. These peptides include the orexigenic peptide ghrelin and anorexigenic gut peptides peptide YY (PYY) and glucagon-like peptide-1 (GLP-1). For example, lower fasting ghrelin levels, lower postprandial ghrelin suppression, and blunted PYY and GLP-1 responses to food intake could contribute to a dysregulation of appetite in already obese children and adolescents. Whereas, changes in these peptides observed during puberty could facilitate growth. A greater understanding of the major moderating factors of appetite-related peptides in the pediatric population is essential to improve interpretation of study findings and for effective tailoring of strategies targeting appetite control to individuals. While more studies are needed, there is some evidence to suggest that exercise-based lifestyle interventions could be a potential therapeutic strategy to improve appetite-peptide profiles in overweight and obese children and adolescents. The aim of this review is (i) to discuss the potential moderating factors of ghrelin, PYY, and GLP-1, including age and puberty, sex, race and body composition; and (ii) to examine the effects of exercise interventions on these appetite-related gut peptides in children and adolescents.
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4.
Gastrointestinal hormones and polycystic ovary syndrome.
Ma, J, Lin, TC, Liu, W
Endocrine. 2014;(3):668-78
Abstract
Polycystic ovary syndrome (PCOS) is an endocrine disease of women in reproductive age. It is characterized by anovulation and hyperandrogenism. Most often patients with PCOS have metabolic abnormalities such as dyslipidemia, insulin resistance, and glucose intolerance. It is not surprising that obesity is high prevalent in PCOS. Over 60 % of PCOS women are obese or overweight. Modulation of appetite and energy intake is essential to maintain energy balance and body weight. The gastrointestinal tract, where nutrients are digested and absorbed, plays a central role in energy homeostasis. The signals from the gastrointestinal tract arise from the stomach (ghrelin release), proximal small intestine (CCK release), and distal small intestine (GLP-1 and PYY) in response to food. These hormones are recognized as "appetite regulatory hormones." Weight loss is the key in the treatments of obese/overweight patients with PCOS. However, current non-pharmacologic management of body weight is hard to achieve. This review highlighted the gastrointestinal hormones, and discussed the potential strategies aimed at modifying hormones for treatment in PCOS.
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5.
Acute exercise and hormones related to appetite regulation: a meta-analysis.
Schubert, MM, Sabapathy, S, Leveritt, M, Desbrow, B
Sports medicine (Auckland, N.Z.). 2014;(3):387-403
Abstract
BACKGROUND Understanding of the impact of an acute bout of exercise on hormones involved in appetite regulation may provide insight into some of the mechanisms that regulate energy balance. In resting conditions, acylated ghrelin is known to stimulate food intake, while hormones such as peptide YY (PYY), pancreatic polypeptide (PP) and glucagon-like peptide 1 (GLP-1) are known to suppress food intake. OBJECTIVE The objective of this review was to determine the magnitude of exercise effects on levels of gastrointestinal hormones related to appetite, using systematic review and meta-analysis. Additionally, factors such as the exercise intensity, duration and mode, in addition to participant characteristics, were examined to determine their influence on these hormones. DATA SOURCES Major databases (PubMed, Scopus, Google Scholar, Science Direct, Academic Search Premier and EBSCOHost) were searched, through February 2013, for original studies, abstracts, theses and dissertations that examined responses of appetite hormones to acute exercise. STUDY SELECTION Studies were included if they evaluated appetite hormone responses during and in the hours after an acute bout of exercise and reported area under the concentration-time curve (AUC) values for more than three datapoints. Studies reporting mean or pre/post-values only were excluded. STUDY APPRAISAL AND SYNTHESIS Initially, 75 studies were identified. After evaluation of study quality and validity, using the Physiotherapy Evidence Database scale, data from 20 studies (28 trials) involving 241 participants (77.6 % men) had their data extracted for inclusion in the meta-analyses. A random-effects meta-analysis was conducted for acylated ghrelin (n = 18 studies, 25 trials) and PYY (n = 8 studies, 14 trials), with sub-group analyses and meta-regressions being conducted for moderator variables. Because the number of studies was limited, fixed-effects meta-analyses were performed on PP data (n = 4 studies, 5 trials) and GLP-1 data (n = 5 studies, 8 trials). RESULTS The results of the meta-analyses indicated that exercise had small to moderate effects on appetite hormone levels, suppressing acylated ghrelin (effect size [ES] Cohen's d value -0.20, 95 % confidence interval [CI] -0.373 to -0.027; median decrease 16.5 %) and increasing PYY (ES 0.24, 95 % CI 0.007 to 0.475; median increase 8.9 %), GLP-1 (ES 0.275, 95 % CI -0.031 to 0.581; median increase 13 %), and PP (ES 0.50, 95 % CI 0.11 to 0.89; median increase 15 %). No significant heterogeneity was detected in any meta-analysis (using Cochrane's Q and I (2)); however, publication biases were detected for all analyses. No moderator variables were observed to moderate the variability among the studies assessing acylated ghrelin and PYY. LIMITATIONS The majority of the present literature is acute in nature; therefore, longer-term alterations in appetite hormone concentrations and their influence on food and beverage intake are unknown. Furthermore, our review was limited to English-language studies and studies reporting AUC data. CONCLUSIONS An acute bout of exercise may influence appetite by suppressing levels of acylated ghrelin while simultaneously increasing levels of PYY, GLP-1 and PP, which may contribute to alterations in food and drink intake after acute exercise. Further longitudinal studies and exploration into mechanisms of action are required in order to determine the precise role these hormones play in long-term appetite responses to an exercise intervention.
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6.
From endocrine to rheumatism: do gut hormones play roles in rheumatoid arthritis?
Chen, CY, Tsai, CY
Rheumatology (Oxford, England). 2014;(2):205-12
Abstract
RA is characterized by chronic inflammation in the musculoskeletal system, in which TNF-α is the key cytokine trigger. TNF-α, previously known as cachectin, is implicated in the modulation of body composition and energy expenditure. Gut hormones, including acyl ghrelin, des-acyl ghrelin, GIP, GLP-1 and PYY, have been known to be the major regulators of appetite, nutrition, energy expenditure and body mass formation. Emerging evidence indicates that blockade of TNF-α by biologics not only ameliorates rheumatoid inflammation, but can affect the secretion and action of gut hormones on appetite, body composition, energy expenditure, muscle catabolism and bone remodelling. A link between the gastrointestinal endocrine axis and the immune system may be established through the interaction of proinflammatory cytokines, including TNF-α and these gut hormones. With the ever-increasing understanding of rheumatoid inflammation and the invention of more biologics to modulate the cytokine network, more attention should be given to the possible immunomodulatory roles of gut hormones in autoimmune inflammatory reactions.
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7.
The interaction of amylin with other hormones in the control of eating.
Lutz, TA
Diabetes, obesity & metabolism. 2013;(2):99-111
Abstract
Twenty years of research established amylin as an important control of energy homeostasis. Amylin controls nutrient and energy fluxes by reducing energy intake, by modulating nutrient utilization via an inhibition of postprandial glucagon secretion and by increasing energy disposal via a prevention of compensatory decreases of energy expenditure in weight reduced individuals. Like many other gastrointestinal hormones, amylin is secreted in response to meals and it reduces eating by promoting meal-ending satiation. Not surprisingly, amylin interacts with many of these hormones to control eating. These interactions seem to occur at different levels because amylin seems to mediate the eating inhibitory effect of some of these gastrointestinal hormones, and the combination of some of these hormones seems to lead to a stronger reduction in eating than single hormones alone. Amylin's effect on eating is thought to be mediated by a stimulation of specific amylin receptors in the area postrema. Secondary brain sites that were defined to mediate amylin action - and hence potential additional sites of interaction with other hormones - include the nucleus of the solitary tract, the lateral parabrachial nucleus, the lateral hypothalamic area and other hypothalamic nuclei. The focus of this review is to summarize the current knowledge of amylin interactions in the control of eating. In most cases, these interactions have only been studied at a descriptive rather than a mechanistic level and despite the clear knowledge on primary sites of amylin action, the interaction sites between amylin and other hormones are often unknown.
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8.
Peptide YY in children: a review.
Wojcicki, JM
Journal of pediatric endocrinology & metabolism : JPEM. 2012;(3-4):227-32
Abstract
BACKGROUND Peptide YY has been found to reduce food intake via the vagal-brainstem-hypothalamic pathway. There is some indication that PYY levels may differ in early childhood in comparison with adult studies. Studies of PYY in children have yet to be synthesized. METHODS This review synthesized 21 articles including studies with infants/newborns, primary school age children and populations with special health needs. RESULTS Some important differences emerge between studies of PYY in children in comparison to those with adults. In those studies with infants and newborns, there is a high level of PYY in preterm and full-term neonates in comparison with school age children and adults. As children get older the relationship between PYY levels and body composition and obesity is more similar to that of adults. Fasting PYY levels may be lower in obese children in comparison with adults and weight loss may restore a higher postprandial level of PYY in contrast with adults whose levels remain low. CONCLUSIONS Additional studies are needed to better understand the role of higher PYY in infancy and to assess the effectiveness of different diets on children throughout time-points in growth and development as well as those with different racial/ethnic background.
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9.
Ghrelin, the proglucagon-derived peptides and peptide YY in nutrient homeostasis.
Dong, CX, Brubaker, PL
Nature reviews. Gastroenterology & hepatology. 2012;(12):705-15
Abstract
Dysregulation of nutrient homeostasis is implicated in the current epidemics of obesity and type 2 diabetes mellitus. The maintenance of homeostasis in the setting of repeated cycles of feeding and fasting occurs through complex interactions between metabolic, hormonal and neural factors. Although pancreatic islets, the liver, muscle, adipocytes and the central nervous system are all key players in this network, the gastrointestinal tract is the first tissue exposed to ingested nutrients and thus has an important role. This Review focuses on several of the endocrine hormones released by the gastrointestinal tract prior to or during nutrient ingestion that have key roles in maintaining energy balance. These hormones include the gastric orexigenic hormone, ghrelin, and the distal L cell anorexigenic and metabolic hormones, glucagon-like peptide (GLP)-1, GLP-2, oxyntomodulin and peptide YY. Each of these hormones exerts a distinct set of biological actions to maintain nutrient homeostasis, the properties of which are currently, or might soon be, exploited in the clinic for the treatment of obesity and type 2 diabetes mellitus.
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10.
Gastrointestinal hormonal dysfunction in gastroparesis and functional dyspepsia.
Khoo, J, Rayner, CK, Feinle-Bisset, C, Jones, KL, Horowitz, M
Neurogastroenterology and motility. 2010;(12):1270-8
Abstract
BACKGROUND Numerous hormones secreted by the gut, during both the fasted state and in response to a meal, influence gastrointestinal motor and/or sensory function, and appear to contribute to the pathogenesis of delayed gastric emptying associated with gastroparesis, functional dyspepsia (FD) and feed intolerance in critical illness. Gut hormones are, accordingly, potential targets for the management of these patients. PURPOSE This article will discuss the hypersensitivity to enteral fat and endogenous (nutrient-stimulated) and exogenous cholecystokinin (CCK) in patients with FD, and the elevation in both fasting and postprandial CCK levels evident in this group. It will review the use of pharmacological agonists of motilin and ghrelin, which accelerate gastric emptying, in the management of gastroparesis and FD. The frequent finding of markedly delayed gastric emptying in the critically ill will be examined; this is associated with elevated plasma CCK and peptide YY in both the fasted and postprandial states, which may account for the increase in small intestinal nutrient inhibitory feedback on gastric motility in this group. The concepts that the rate of gastric emptying is a major determinant of postprandial glycemic excursions in diabetes, and that modulation of gastric emptying may improve glycemic control, will be addressed; in type 1 and insulin-treated type 2 diabetic patients, co-ordination of insulin administration with nutrient delivery and absorption should be optimized, while type 2 patients who are not on insulin are likely to respond to dietary and/or pharmacological interventions which slow gastric emptying.