scholarly journals The Gut Hormones in Appetite Regulation

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Keisuke Suzuki ◽  
Channa N. Jayasena ◽  
Stephen R. Bloom
Keyword(s):  
Bariatric Surgery ◽  
Weight Loss ◽  
Food Intake ◽  
Peptide Yy ◽  
Critical Role ◽  
Gut Hormones ◽  
Energy Status ◽  
Increased Risk ◽  
Glucagon Like Peptide 1

Obesity has received much attention worldwide in association with an increased risk of cardiovascular diseases, diabetes, and cancer. At present, bariatric surgery is the only effective treatment for obesity in which long-term weight loss is achieved in patients. By contrast, pharmacological interventions for obesity are usually followed by weight regain. Although the exact mechanisms of long-term weight loss following bariatric surgery are yet to be fully elucidated, several gut hormones have been implicated. Gut hormones play a critical role in relaying signals of nutritional and energy status from the gut to the central nervous system, in order to regulate food intake. Cholecystokinin, peptide YY, pancreatic polypeptide, glucagon-like peptide-1, and oxyntomodulin act through distinct yet synergistic mechanisms to suppress appetite, whereas ghrelin stimulates food intake. Here, we discuss the role of gut hormones in the regulation of food intake and body weight.

scholarly journals How Satiating Are the ‘Satiety’ Peptides: A Problem of Pharmacology versus Physiology in the Development of Novel Foods for Regulation of Food Intake

Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1517 ◽  
Author(s):  
Jia Jiet Lim ◽  
Sally D. Poppitt
Keyword(s):  
Weight Loss ◽  
Food Intake ◽  
Energy Intake ◽  
Peptide Yy ◽  
Behavioural Change ◽  
Eating Behaviour ◽  
Predictive Biomarkers ◽  
Negative Energy ◽  
Novel Foods ◽  
Glucagon Like Peptide 1

Developing novel foods to suppress energy intake and promote negative energy balance and weight loss has been a long-term but commonly unsuccessful challenge. Targeting regulation of appetite is of interest to public health researchers and industry in the quest to develop ‘functional’ foods, but poor understanding of the underpinning mechanisms regulating food intake has hampered progress. The gastrointestinal (GI) or ‘satiety’ peptides including cholecystokinin (CCK), glucagon-like peptide 1 (GLP-1) and peptide YY (PYY) secreted following a meal, have long been purported as predictive biomarkers of appetite response, including food intake. Whilst peptide infusion drives a clear change in hunger/fullness and eating behaviour, inducing GI-peptide secretion through diet may not, possibly due to modest effects of single meals on peptide levels. We conducted a review of 70 dietary preload (DIET) and peptide infusion (INFUSION) studies in lean healthy adults that reported outcomes of CCK, GLP-1 and PYY. DIET studies were acute preload interventions. INFUSION studies showed that minimum increase required to suppress ad libitum energy intake for CCK, GLP-1 and PYY was 3.6-, 4.0- and 3.1-fold, respectively, achieved through DIET in only 29%, 0% and 8% of interventions. Whether circulating ‘thresholds’ of peptide concentration likely required for behavioural change can be achieved through diet is questionable. As yet, no individual or group of peptides can be measured in blood to reliably predict feelings of hunger and food intake. Developing foods that successfully target enhanced secretion of GI-origin ‘satiety’ peptides for weight loss remains a significant challenge.

scholarly journals Peptide YY, appetite and food intake

2005 ◽  
Vol 64 (2) ◽  
pp. 213-216 ◽  
Author(s):  
C. W. le Roux ◽  
S. R. Bloom
Keyword(s):  
Food Intake ◽  
Peptide Yy ◽  
Energy Content ◽  
Peak Plasma ◽  
Evolutionary Relationship ◽  
Gut Hormones ◽  
Amino Acid Peptide ◽  
Control Food ◽  
Glucagon Like Peptide 1 ◽  
Control Food Intake

Obesity is taking on pandemic proportions. The laws of thermodynamics, however, remain unchanged, as energy will be stored if less energy is expended than consumed; the storage is usually in the form of adipose tissue. Several neural, humeral and psychological factors control the complex process known as appetite. Recently, a close evolutionary relationship between the gut and brain has become apparent. The gut hormones regulate important gastrointestinal functions such as motility, secretion, absorption, provide feedback to the central nervous system on availability of nutrients and may play a part in regulating food intake. Peptide YY (PYY) is a thirty-six amino acid peptide related to neuropeptide Y (NPY) and is co-secreted with glucagon-like peptide 1. Produced by the intestinal L-cells, the highest tissue concentrations of PYY are found in distal segments of the gastrointestinal tract, although it is present throughout the gut. Following food intake PYY is released into the circulation. PYY concentrations are proportional to meal energy content and peak plasma levels appear postprandially after 1 h. PYY3-36 is a major form of PYY in both the gut mucosal endocrine cells and the circulation. Peripheral administration of PYY3-36 inhibits food intake for several hours in both rodents and man. The binding of PYY3-36 to the Y2 receptor leads to an inhibition of the NPY neurones and a possible reciprocal stimulation of the pro-opiomelanocortin neurones. Thus, PYY3-36 appears to control food intake by providing a powerful feedback on the hypothalamic circuits. The effect on food intake has been demonstrated at physiological concentrations and, therefore, PYY3-36 may be important in the everyday regulation of food intake.

scholarly journals MANAGEMENT OF ENDOCRINE DISEASE: Metabolic effects of bariatric surgery

2016 ◽  
Vol 174 (1) ◽  
pp. R19-R28 ◽  
Author(s):  
Ricard Corcelles ◽  
Christopher R Daigle ◽  
Philip R Schauer
Keyword(s):  
Cardiovascular Disease ◽  
Bariatric Surgery ◽  
Metabolic Syndrome ◽  
Weight Loss ◽  
Metabolic Effects ◽  
Perioperative Morbidity ◽  
Increased Risk ◽  
Long Term Impact

Obesity is associated with an increased risk of type 2 diabetes, hypertension, dyslipidemia, cardiovascular disease, osteoarthritis, numerous cancers and increased mortality. It is estimated that at least 2.8 million adults die each year due to obesity-related cardiovascular disease. Increasing in parallel with the global obesity problem is metabolic syndrome, which has also reached epidemic levels. Numerous studies have demonstrated that bariatric surgery is associated with significant and durable weight loss with associated improvement of obesity-related comorbidities. This review aims to summarize the effects of bariatric surgery on the components of metabolic syndrome (hyperglycemia, hyperlipidemia and hypertension), weight loss, perioperative morbidity and mortality, and the long-term impact on cardiovascular risk and mortality.

scholarly journals The Effect of a Subcutaneous Infusion of GLP-1, OXM, and PYY on Energy Intake and Expenditure in Obese Volunteers

2017 ◽  
Vol 102 (7) ◽  
pp. 2364-2372 ◽  
Author(s):  
Tricia Tan ◽  
Preeshila Behary ◽  
George Tharakan ◽  
James Minnion ◽  
Werd Al-Najim ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Energy Intake ◽  
Peptide Yy ◽  
Gut Hormones ◽  
Resting Energy Expenditure ◽  
Subcutaneous Infusion ◽  
Glucagon Like Peptide 1 ◽  
Treatment Of Obesity ◽  
First Time

Abstract Background: Roux-en-Y gastric bypass (RYGB) surgery is currently the most effective treatment of obesity, although limited by availability and operative risk. The gut hormones Glucagon-like peptide-1 (GLP-1), Peptide YY (PYY), and Oxyntomodulin (OXM) are elevated postprandially after RYGB, which has been postulated to contribute to its metabolic benefits. Objective: We hypothesized that infusion of the three gut hormones to achieve levels similar to those encountered postprandially in RYGB patients might be effective in suppressing appetite. The aim of this study was to investigate the effect of a continuous infusion of GLP-1, OXM, and PYY (GOP) on energy intake and expenditure in obese volunteers. Methods: Obese volunteers were randomized to receive an infusion of GOP or placebo in a single-blinded, randomized, placebo-controlled crossover study for 10.5 hours a day. This was delivered subcutaneously using a pump device, allowing volunteers to remain ambulatory. Ad libitum food intake studies were performed during the infusion, and energy expenditure was measured using a ventilated hood calorimeter. Results: Postprandial levels of GLP-1, OXM, and PYY seen post RYGB were successfully matched using 4 pmol/kg/min, 4 pmol/kg/min, and 0.4 pmol/kg/min, respectively. This dose led to a mean reduction of 32% in food intake. No significant effects on resting energy expenditure were observed. Conclusion: This is, to our knowledge, the first time that an acute continuous subcutaneous infusion of GOP, replicating the postprandial levels observed after RYGB, is shown to be safe and effective in reducing food intake. This data suggests that triple hormone therapy might be a useful tool against obesity.

scholarly journals Obesity and Appetite Control

2012 ◽  
Vol 2012 ◽  
pp. 1-19 ◽  
Author(s):  
Keisuke Suzuki ◽  
Channa N. Jayasena ◽  
Stephen R. Bloom
Keyword(s):  
Food Intake ◽  
Energy Homeostasis ◽  
Peptide Yy ◽  
Gut Hormones ◽  
Appetite Control ◽  
Control Food ◽  
Adiposity Signals ◽  
Term Energy ◽  
Glucagon Like Peptide 1 ◽  
Control Food Intake

Obesity is one of the major challenges to human health worldwide; however, there are currently no effective pharmacological interventions for obesity. Recent studies have improved our understanding of energy homeostasis by identifying sophisticated neurohumoral networks which convey signals between the brain and gut in order to control food intake. The hypothalamus is a key region which possesses reciprocal connections between the higher cortical centres such as reward-related limbic pathways, and the brainstem. Furthermore, the hypothalamus integrates a number of peripheral signals which modulate food intake and energy expenditure. Gut hormones, such as peptide YY, pancreatic polypeptide, glucagon-like peptide-1, oxyntomodulin, and ghrelin, are modulated by acute food ingestion. In contrast, adiposity signals such as leptin and insulin are implicated in both short- and long-term energy homeostasis. In this paper, we focus on the role of gut hormones and their related neuronal networks (the gut-brain axis) in appetite control, and their potentials as novel therapies for obesity.

PYY3-36 injection in mice produces an acute anorexigenic effect followed by a delayed orexigenic effect not observed with other anorexigenic gut hormones

2008 ◽  
Vol 294 (4) ◽  
pp. E698-E708 ◽  
Author(s):  
James R. C. Parkinson ◽  
Waljit S. Dhillo ◽  
Caroline J. Small ◽  
Owais B. Chaudhri ◽  
Gavin A. Bewick ◽  
...  
Keyword(s):  
Food Intake ◽  
Peptide Yy ◽  
Gut Hormones ◽  
Reduce Food Intake ◽  
Dark Phase ◽  
Light Phase ◽  
Show Evidence ◽  
Ad Libitum ◽  
Glucagon Like Peptide 1 ◽  
Anorexigenic Effect

Peptide YY (PYY) is secreted postprandially from the endocrine L cells of the gastrointestinal tract. PYY3-36, the major circulating form of the peptide, is thought to reduce food intake in humans and rodents via high-affinity binding to the autoinhibitory neuropeptide Y (NPY) receptor within the arcuate nucleus. We studied the effect of early light-phase injection of PYY3-36 on food intake in mice fasted for 0, 6, 12, 18, 24, and 30 h and show that PYY3-36 produces an acute anorexigenic effect regardless of the duration of fasting. We also show evidence of a delayed orexigenic effect in ad libitum-fed mice injected with PYY3-36 in the early light phase. This delayed orexigenic effect also occurs in mice administered a potent analog of PYY3-36, d-Allo Ile3 PYY3-36, but not following injection of other anorectic agents (glucagon-like-peptide 1, oxyntomodulin, and lithium chloride). Early light-phase injection of PYY3-36 to ad libitum-fed mice resulted in a trend toward increased levels of hypothalamic NPY and agouti-related peptide mRNA and a decrease in proopiomelanocortin mRNA at the beginning of the dark phase. Furthermore, plasma levels of ghrelin were increased significantly, and there was a trend toward decreased plasma PYY3-36 levels at the beginning of the dark phase. These data indicate that PYY3-36 injection results in an acute anorexigenic effect followed by a delayed orexigenic effect.

scholarly journals Role of capsaicin-sensitive peripheral sensory neurons in anorexic responses to intravenous infusions of cholecystokinin, peptide YY-(3–36), and glucagon-like peptide-1 in rats

2014 ◽  
Vol 307 (8) ◽  
pp. E619-E629 ◽  
Author(s):  
Roger Reidelberger ◽  
Alvin Haver ◽  
Krista Anders ◽  
Bettye Apenteng
Keyword(s):  
Food Intake ◽  
Sensory Neurons ◽  
Peptide Yy ◽  
Gut Hormones ◽  
Intravenous Infusions ◽  
Peripheral Sensory Neurons ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Peripheral Sensory ◽  
Infusion Period

Cholecystokinin (CCK)-induced suppression of feeding is mediated by vagal sensory neurons that are destroyed by the neurotoxin capsaicin (CAP). Here we determined whether CAP-sensitive neurons mediate anorexic responses to intravenous infusions of gut hormones peptide YY-(3–36) [PYY-(3–36)] and glucagon-like peptide-1 (GLP-1). Rats received three intraperitoneal injections of CAP or vehicle (VEH) in 24 h. After recovery, non-food-deprived rats received at dark onset a 3-h intravenous infusion of CCK-8 (5, 17 pmol·kg−1·min−1), PYY-(3–36) (5, 17, 50 pmol·kg−1·min−1), or GLP-1 (17, 50 pmol·kg−1·min−1). CCK-8 was much less effective in reducing food intake in CAP vs. VEH rats. CCK-8 at 5 and 17 pmol·kg−1·min−1 reduced food intake during the 3-h infusion period by 39 and 71% in VEH rats and 7 and 18% in CAP rats. In contrast, PYY-(3–36) and GLP-1 were similarly effective in reducing food intake in VEH and CAP rats. PYY-(3–36) at 5, 17, and 50 pmol·kg−1·min−1 reduced food intake during the 3-h infusion period by 15, 33, and 70% in VEH rats and 13, 30, and 33% in CAP rats. GLP-1 at 17 and 50 pmol·kg−1·min−1 reduced food intake during the 3-h infusion period by 48 and 60% in VEH rats and 30 and 52% in CAP rats. These results suggest that anorexic responses to PYY-(3–36) and GLP-1 are not primarily mediated by the CAP-sensitive peripheral sensory neurons (presumably vagal) that mediate CCK-8-induced anorexia.

scholarly journals Successful weight loss maintenance includes long-term increased meal responses of GLP-1 and PYY3–36

2016 ◽  
Vol 174 (6) ◽  
pp. 775-784 ◽  
Author(s):  
Eva W Iepsen ◽  
Julie Lundgren ◽  
Jens J Holst ◽  
Sten Madsbad ◽  
Signe S Torekov
Keyword(s):  
Weight Loss ◽  
Peptide Yy ◽  
Weight Maintenance ◽  
Area Under The Curve ◽  
Weight Loss Maintenance ◽  
Very Low Calorie Diet ◽  
Calorie Diet ◽  
Glucagon Like Peptide 1 ◽  
Successful Weight Loss

ObjectiveThe hormones glucagon-like peptide 1 (GLP-1), peptide YY3-36(PYY3–36), ghrelin, glucose-dependent insulinotropic polypeptide (GIP) and glucagon have all been implicated in the pathogenesis of obesity. However, it is unknown whether they exhibit adaptive changes with respect to postprandial secretion to a sustained weight loss.DesignThe study was designed as a longitudinal prospective intervention study with data obtained at baseline, after 8 weeks of weight loss and 1 year after weight loss.MethodsTwenty healthy obese individuals obtained a 13% weight loss by adhering to an 8-week very low-calorie diet (800kcal/day). After weight loss, participants entered a 52-week weight maintenance protocol. Plasma levels of GLP-1, PYY3–36, ghrelin, GIP and glucagon during a 600-kcal meal were measured before weight loss, after weight loss and after 1 year of weight maintenance. Area under the curve (AUC) was calculated as total AUC (tAUC) and incremental AUC (iAUC).ResultsWeight loss was successfully maintained for 52 weeks. iAUC for GLP-1 increased by 44% after weight loss (P<0.04) and increased to 72% at week 52 (P=0.0001). iAUC for PYY3–36increased by 74% after weight loss (P<0.0001) and by 36% at week 52 (P=0.02). tAUC for ghrelin increased by 23% after weight loss (P<0.0001), but at week 52, the increase was reduced to 16% compared with before weight loss (P=0.005). iAUC for GIP increased by 36% after weight loss (P=0.001), but returned to before weight loss levels at week 52. Glucagon levels were unaffected by weight loss.ConclusionsMeal responses of GLP-1 and PYY3–36remained increased 1 year after weight maintenance, whereas ghrelin and GIP reverted toward before-weight loss values. Thus, an increase in appetite inhibitory mechanisms and a partly decrease in appetite-stimulating mechanisms appear to contribute to successful long-term weight loss maintenance.

scholarly journals Food Intake and Eating Behavior After Bariatric Surgery

2018 ◽  
Vol 98 (3) ◽  
pp. 1113-1141 ◽  
Author(s):  
Werd Al-Najim ◽  
Neil G. Docherty ◽  
Carel W. le Roux
Keyword(s):  
Bariatric Surgery ◽  
Food Intake ◽  
Eating Behavior ◽  
Synergistic Effects ◽  
Gut Hormones ◽  
Physiological Changes ◽  
Long Term Outcomes ◽  
Profound Influence ◽  
Efficacious Treatment

Obesity is an escalating global chronic disease. Bariatric surgery is a very efficacious treatment for obesity and its comorbidities. Alterations to gastrointestinal anatomy during bariatric surgery result in neurological and physiological changes affecting hypothalamic signaling, gut hormones, bile acids, and gut microbiota, which coalesce to exert a profound influence on eating behavior. A thorough understanding of the mechanisms underlying eating behavior is essential in the management of patients after bariatric surgery. Studies investigating candidate mechanisms have expanded dramatically in the last decade. Herein we review the proposed mechanisms governing changes in eating behavior, food intake, and body weight after bariatric surgery. Additive or synergistic effects of both conditioned and unconditioned factors likely account for the complete picture of changes in eating behavior. Considered application of strategies designed to support the underlying principles governing changes in eating behavior holds promise as a means of optimizing responses to surgery and long-term outcomes.

scholarly journals Sir David Cuthbertson Medal Lecture Bariatric surgery as a model to study appetite control

2009 ◽  
Vol 68 (3) ◽  
pp. 227-233 ◽  
Author(s):  
Marco Bueter ◽  
Carel W. le Roux
Keyword(s):  
Bariatric Surgery ◽  
Peptide Yy ◽  
Gastrointestinal Hormones ◽  
Gut Hormones ◽  
Gastric Inhibitory Polypeptide ◽  
Appetite Regulation ◽  
Appetite Control ◽  
Obesity Epidemic ◽  
Glucagon Like Peptide 1 ◽  
Underlying Mechanisms

The obesity epidemic and its associated morbidity and mortality have led to major research efforts to identify mechanisms that regulate appetite. Gut hormones have recently been found to be an important element in appetite regulation as a result of the signals from the periphery to the brain. Candidate hormones include ghrelin, peptide YY, glucagon-like peptide-1 and gastric inhibitory polypeptide, all of which are currently being investigated as potential obesity treatments. Bariatric surgery is currently the most effective therapy for substantial and sustained weight loss. Understanding how levels of gut hormones are modulated by such procedures has greatly contributed to the comprehension of the underlying mechanisms of appetite and obesity. The present paper is a review of how appetite and levels of gastrointestinal hormones are altered after bariatric surgery. Basic principles of common bariatric procedures and potential mechanisms for appetite regulation by gut hormones are also addressed.

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