Effect of a protein preload on food intake and satiety feelings in response to duodenal fat perfusions in healthy male subjects

2005 ◽  
Vol 289 (4) ◽  
pp. R1042-R1047 ◽  
Author(s):  
Sibylle Oesch ◽  
Lukas Degen ◽  
Christoph Beglinger
Keyword(s):  
Food Intake ◽  
Synergistic Effect ◽  
Peptide Yy ◽  
Caloric Intake ◽  
Healthy Male ◽  
Double Blind ◽  
Control Food ◽  
Initial Hypothesis ◽  
Glucagon Like Peptide 1 ◽  
Control Food Intake

The control of food intake and satiety requires a coordinated interplay. Oral protein and duodenal fat inhibit food intake and induce satiety, but their interactive potential is unclear. Our aim was therefore to investigate the interactions between an oral protein preload and intraduodenal (ID) fat on food intake and satiety feelings. Twenty healthy male volunteers were studied in a randomized, double-blind, four-period crossover design. On each study day, subjects underwent one of the following treatments: 1) water preload plus ID saline perfusion, 2) water preload plus ID fat perfusion, 3) protein preload plus ID saline perfusion, or 4) protein preload plus ID fat perfusion. Subjects were free to eat and drink as much as they wished. An oral protein preload significantly reduced caloric intake (19%, P < 0.01). Simultaneous administration of an oral protein preload and ID fat did not result in a positive synergistic effect with respect to caloric consumption, rejecting the initial hypothesis that the two nutrients exert a positive synergistic effect on food intake. An oral protein preload but not ID fat altered the feelings of hunger and fullness. These data indicate that the satiety effect of an oral protein preload is not amplified by ID fat; indeed, the effect of a protein preload does not seem to be mediated by cholecystokinin, glucagon-like peptide-1, or peptide YY. Much more information is necessary to understand the basic physiological mechanisms that control food intake and satiety.

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 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.

Mechanisms behind GLP-1 induced weight loss

2008 ◽  
Vol 8 (2_suppl) ◽  
pp. S34-S41 ◽  
Author(s):  
Philip J Larsen
Keyword(s):  
Energy Homeostasis ◽  
Caloric Intake ◽  
Underlying Mechanism ◽  
Negative Energy ◽  
Incretin Hormone ◽  
Dipeptidyl Peptidase 4 ◽  
Control Food ◽  
The Central Nervous System ◽  
Glucagon Like Peptide 1 ◽  
Control Food Intake

Endogenous glucagon-like peptide-1 (GLP-1) is an incretin hormone that plays an important role in maintaining pancreatic function as well as caloric intake. Since the advent of GLP-1 receptor agonists resistant to dipeptidyl peptidase-4 (DPP-4) (degradation, it has become clear that their chronic use promotes negative energy balance. With regard to their effects on body weight, the principal action of GLP-1 agonists is mediated via their inhibition of eating. In searching for the underlying mechanism of GLP-1 receptor agonist-induced anorexic effect, scientists have discovered pathways in the central nervous system, as well as in the periphery. This review describes emerging knowledge of a peripheral endocrine GLP-1 system mediating its activity through a central ascending GLP-1 pathway and targeting hypothalamic sites involved in the regulation of energy homeostasis. Thus peripheral and central GLP-1 sensitive pathways appear to be organised to co-operatively help control food intake and body weight.Br J Diabetes Vasc Dis 2008;8 (Suppl 2): S34—S41

scholarly journals NPY2 receptor activation in the dorsal vagal complex increases food intake and attenuates CCK-induced satiation in male rats

2019 ◽  
Vol 316 (4) ◽  
pp. R406-R416
Author(s):  
Nathaneal J. Huston ◽  
Lynne A. Brenner ◽  
Zachary C. Taylor ◽  
Robert C. Ritter
Keyword(s):  
Food Intake ◽  
Peptide Yy ◽  
Receptor Activation ◽  
Vagal Afferents ◽  
Male Rats ◽  
Dorsal Vagal Complex ◽  
Increase Food Intake ◽  
Control Food ◽  
Intracerebroventricular Injections ◽  
Control Food Intake

Neuropeptide Y (NPY), peptide YY (PYY), and their cognate receptors (YR) are expressed by subpopulations of central and peripheral nervous system neurons. Intracerebroventricular injections of NPY or PYY increase food intake, and intrahypothalamic NPY1 or NPY5 receptor agonist injections also increase food intake. In contrast, injection of PYY in the periphery reduces food intake, apparently by activating peripheral Y2R. The dorsal vagal complex (DVC) of the hindbrain is the site where vagal afferents relay gut satiation signals to the brain. While contributions of the DVC are increasingly investigated, a role for DVC YR in control of food intake has not been examined systematically. We used in situ hybridization to confirm expression of Y1R and Y2R, but not Y5R, in the DVC and vagal afferent neurons. We found that nanoinjections of a Y2R agonist, PYY-(3–36), into the DVC significantly increased food intake over a 4-h period in satiated male rats. PYY-(3–36)-evoked food intake was prevented by injection of a selective Y2R antagonist. Injection of a Y1R/Y5R-preferring agonist into the DVC failed to increase food intake at doses reported to increase food intake following hypothalamic injection. Finally, injection of PYY-(3–36) into the DVC prevented reduction of 30-min food intake following intraperitoneal injection of cholecystokinin (CCK). Our results indicate that activation of DVC Y2R, unlike hypothalamic or peripheral Y2R, increases food intake. Furthermore, in the context of available electrophysiological observations, our results are consistent with the hypothesis that DVC Y2R control food intake by dampening vagally mediated satiation signals in the DVC.

scholarly journals Oral administration of glucagon-like peptide 1 or peptide YY 3-36 affects food intake in healthy male subjects

2010 ◽  
Vol 92 (4) ◽  
pp. 810-817 ◽  
Author(s):  
Robert E Steinert ◽  
Birk Poller ◽  
M Cristina Castelli ◽  
Juergen Drewe ◽  
Christoph Beglinger
Keyword(s):  
Food Intake ◽  
Oral Administration ◽  
Peptide Yy ◽  
Healthy Male ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Male Subjects

Peptide YY and glucagon-like peptide-1 contribute to decreased food intake after Roux-en-Y gastric bypass surgery

2016 ◽  
Vol 40 (11) ◽  
pp. 1699-1706 ◽  
Author(s):  
M S Svane ◽  
N B Jørgensen ◽  
K N Bojsen-Møller ◽  
C Dirksen ◽  
S Nielsen ◽  
...  
Keyword(s):  
Gastric Bypass ◽  
Food Intake ◽  
Bypass Surgery ◽  
Peptide Yy ◽  
Gastric Bypass Surgery ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

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.

Parenteral nutrition, brain glycogen, and food intake

1993 ◽  
Vol 265 (6) ◽  
pp. R1387-R1391
Author(s):  
M. M. Meguid ◽  
J. L. Beverly ◽  
Z. J. Yang ◽  
J. R. Gleason ◽  
R. A. Meguid ◽  
...  
Keyword(s):  
Food Intake ◽  
Parenteral Nutrition ◽  
Plasma Glucose ◽  
Glycogen Content ◽  
Fischer 344 Rats ◽  
Brain Glycogen ◽  
Fischer 344 ◽  
Control Food ◽  
Control Food Intake ◽  
Infusion Period

To determine whether brain glycogen concentrations change during parenteral nutrition, Fischer 344 rats with jugular vein catheters received 0.9 N saline or parenteral nutrition providing 100% of daily calories (PN-100). Rats were killed after 4 days of PN-100 and serially after PN-100 was stopped. Food intake decreased during PN-100 to approximately 15% of control, but total kilocalories eaten and infused over the 4-day PN-100 period was approximately 130% of control. Food intake of PN-100 rats remained low for 3-4 days post-PN-100. At the end of the 4-day PN-100 period, plasma glucose and insulin (P = 0.01) and whole brain glycogen (P < 0.005) were higher than but similar to control within 24 h of PN-100 being stopped. When PN-100 rats were not allowed to eat during the infusion period, plasma glucose was lower, plasma insulin higher, and brain glycogen content the same as in control rats after 4 days of PN-100. The increased brain glycogen was the likely consequence of the hyperglycemia and hyperinsulinemia during PN-100 and was not causally associated with the reduced food intake either during or immediately after PN-100.

Intermittent intraperitoneal infusion of peptide YY(3-36) reduces daily food intake and adiposity in obese rats

2007 ◽  
Vol 293 (1) ◽  
pp. R39-R46 ◽  
Author(s):  
Prasanth K. Chelikani ◽  
Alvin C. Haver ◽  
Roger D. Reidelberger
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Peptide Yy ◽  
Caloric Intake ◽  
Daily Food Intake ◽  
Daily Caloric Intake ◽  
Intraperitoneal Infusion ◽  
Daily Food ◽  
Sustained Reduction ◽  
Obese Rats

Peptide YY(3-36) [PYY(3-36)] is a gut-brain peptide that decreases food intake when administered by intravenous infusion to lean and obese humans and rats. However, chronic administration of PYY(3-36) by osmotic minipump to lean and obese rodents produces only a transient reduction in daily food intake and weight gain. It has recently been shown that 1-h intravenous infusions of PYY(3-36) every other hour for 10 days produced a sustained reduction in daily food intake, body weight, and adiposity in lean rats. Here, we determined whether intermittent delivery of PYY(3-36) can produce a similar response in diet-induced obese rats. During a 21-day period, obese rats (body fat >25%) received twice daily intraperitoneal infusion of vehicle ( n = 18) or PYY(3-36) ( n = 24) during hours 1–3 and 7–9 of the dark period. Rats had free access to both a 45% fat solid diet and a 29% fat liquid diet; intakes were determined from continuous computer recording of changes in food container weights. To sustain a 15–25% reduction in daily caloric intake, the initial PYY(3-36) dose of 30 pmol·kg−1·min−1 was reduced to 10 pmol·kg−1·min−1 on day 10 and then increased to 17 pmol·kg−1·min−1 on day 13. This dosing strategy produced a sustained reduction in daily caloric intake of 11–32% and prevented body weight gain (8 ± 6 vs. 51 ± 11 g) and fat deposition (4.4 ± 7.6 vs. 41.0 ± 12.8 g). These results indicate that intermittent intraperitoneal infusion of PYY(3-36) can produce a sustained reduction in food intake and adiposity in diet-induced obese rodents consuming palatable high-fat foods.

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