Cholecystokinin receptors and vagal nerves in control of food intake in rats

1990 ◽  
Vol 258 (1) ◽  
pp. E40-E45 ◽  
Author(s):  
J. Garlicki ◽  
P. K. Konturek ◽  
J. Majka ◽  
N. Kwiecien ◽  
S. J. Konturek
Keyword(s):  
Food Intake ◽  
Peptide Yy ◽  
Gastric Inhibitory Polypeptide ◽  
Intragastric Administration ◽  
Gut Peptides ◽  
Sham Feeding ◽  
Liquid Meal ◽  
Vagal Nerves ◽  
Normal Feeding ◽  
Cck Receptor Antagonist

This study was designed to determine the specificity and physiological nature of short-term satiety effects of cholecystokinin (CCK) in rats with intact and transected vagal nerves. Rats with-the gastric fistulas, closed or open, were used for normal feeding or sham feeding of liquid meal offered for 30 min. CCK-8 (0.5-10 nmol/kg) injected intraperitoneally (ip) 15 min before feeding inhibited food intake dose dependently in both normal-fed and sham-fed rats at a minimal inhibitory dose of 1 nmol/kg. CCK-8 at the same doses caused a potent stimulation of pancreatic protein secretion, reaching maximum at a dose of approximately 0.5 nmol/kg. Pretreatment with a potent CCK receptor antagonist, L-364,718 (2.5 mg/kg ip), increased food intake during normal feeding (but not sham feeding) and almost completely blocked the satiety and pancreatic stimulatory effects of CCK. When feeding was preceded by intragastric administration of proteinase inhibitor (Foy-305, 200 mg/kg), food preload, or diversion of bile-pancreatic secretion to the exterior, there was a significant increase in the plasma level of CCK and an inhibition of food intake by about 36, 78, and 25%, respectively. Pretreatment with L-364,718 completely abolished this inhibition by Foy-305 and bile-pancreatic diversion and reduced that caused by food preload. Among other gut peptides given ip (10 nmol/kg) only bombesin reduced food intake, whereas gastrin, secretin, gastric inhibitory polypeptide (GIP), pancreatic polypeptide (PP), and peptide YY (PYY) were ineffective.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Effect of oral or intragastric delivery of the bitter tastant quinine on food intake and appetite sensations: a randomised crossover trial

2020 ◽  
Vol 125 (1) ◽  
pp. 92-100
Author(s):  
Tim Klaassen ◽  
Daniel Keszthelyi ◽  
Annick M. E. Alleleyn ◽  
Ellen Wilms ◽  
Aalt Bast ◽  
...  
Keyword(s):  
Food Intake ◽  
Crossover Trial ◽  
Eating Behaviour ◽  
Intragastric Administration ◽  
Taste Receptors ◽  
Sham Feeding ◽  
Intraduodenal Infusion ◽  
Desire To Eat ◽  
Analogue Scales ◽  
Stimulation Of

AbstractStimulation of gastrointestinal taste receptors affects eating behaviour. Intraduodenal infusion of tastants leads to increased satiation and reduced food intake, whereas intraileal infusion of tastants does not affect eating behaviour. Currently, it is unknown whether oral- or intragastric administration of tastants induces a larger effect on eating behaviour. This study investigated the effects of oral- and/or intragastric administration of quinine on food intake, appetite sensations and heart rate variability (HRV). In a blinded randomised crossover trial, thirty-two healthy volunteers participated in four interventions with a 1-week washout: oral placebo and intragastric placebo (OPGP), oral quinine and intragastric placebo (OQGP), oral placebo and intragastric quinine (OPGQ) and oral quinine and intragastric quinine (OQGQ). On test days, 150 min after a standardised breakfast, subjects ingested a capsule containing quinine or placebo and were sham-fed a mixture of quinine or placebo orally. At 50 min after intervention, subjects received an ad libitum meal to measure food intake. Visual analogue scales for appetite sensations were collected, and HRV measurements were performed at regular intervals. Oral and/or intragastric delivery of the bitter tastant quinine did not affect food intake (OPGP: 3273·6 (sem 131·8) kJ, OQGP: 3072·7 (sem 132·2) kJ, OPGQ: 3289·0 (sem 132·6) kJ and OQGQ: 3204·1 (sem 133·1) kJ, P = 0·069). Desire to eat and hunger decreased after OQGP and OPGQ compared with OPGP (P < 0·001 and P < 0·05, respectively), whereas satiation, fullness and HRV did not differ between interventions. In conclusion, sole oral sham feeding with and sole intragastric delivery of quinine decreased desire to eat and hunger, without affecting food intake, satiation, fullness or HRV.

Appetite-related peptides in childhood and adolescence: role of ghrelin, PYY, and GLP-1

2015 ◽  
Vol 40 (11) ◽  
pp. 1089-1099 ◽  
Author(s):  
Katy Horner ◽  
SoJung Lee
Keyword(s):  
Body Composition ◽  
Food Intake ◽  
Children And Adolescents ◽  
Peptide Yy ◽  
Pediatric Population ◽  
Childhood And Adolescence ◽  
Gut Peptides ◽  
Obese Children ◽  
Exercise Interventions ◽  
Moderating Factors

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.

Effects of atropine on pancreatic response to bethanechol, cholecystokinin, and food intake in rats

1991 ◽  
Vol 261 (5) ◽  
pp. G735-G741
Author(s):  
M. F. O'Rourke ◽  
R. D. Reidelberger ◽  
T. E. Solomon
Keyword(s):  
Food Intake ◽  
Pancreatic Secretion ◽  
Pancreatic Enzyme ◽  
Maximal Response ◽  
Cholinergic Mechanisms ◽  
Liquid Meal ◽  
Amylase Output ◽  
Cck Receptor Antagonist ◽  
The Right

Atropine was used to examine the role of cholinergic mechanisms in the pancreatic secretory response to food intake. Unanesthetized rats with gastric, jugular vein, bile-pancreatic, and duodenal cannulas were used; bile-pancreatic juice was recirculated. The maximal response to bethanechol (4 mg.kg-1.h-1) was similar to cholecystokinin (CCK)-8-induced maximal secretion. Atropine (25-200 micrograms.kg-1.h-1) markedly inhibited basal amylase output and caused dose-related inhibition of the incremental response to a maximal dose of bethanechol. Atropine (50 micrograms.kg-1.h-1) shifted the dose-response curve to bethanechol (1-32 mg.kg-1.h-1) to the right but did not alter maximal amylase output. L 364718 (0.5 mg/kg), a CCK receptor antagonist, had no effect on bethanechol-stimulated pancreatic secretion. Atropine (50 micrograms.kg-1.h-1) did not affect the incremental responses to low doses of CCK-8; the maximal response occurred at a higher CCK-8 dose because atropine decreased basal secretion. Atropine (50 or 200 micrograms.kg-1.h-1) did not decrease the amylase response to ingestion of a liquid meal. We conclude that 1) bethanechol is a full agonist for stimulation of pancreatic enzyme secretion and its effects are not mediated by CCK release; 2) atropine is a competitive antagonist of bethanechol-induced pancreatic secretion in vivo but does not directly affect responses to CCK-8; 3) cholinergic mechanisms do not mediate the pancreatic enzyme response to a liquid meal in rats.

Vagal afferents are not necessary for the satiety effect of the gut lipid messenger oleoylethanolamide

2014 ◽  
Vol 307 (2) ◽  
pp. R167-R178 ◽  
Author(s):  
Elnaz Karimian Azari ◽  
Deepti Ramachandran ◽  
Sandra Weibel ◽  
Myrtha Arnold ◽  
Adele Romano ◽  
...  
Keyword(s):  
Food Intake ◽  
Peptide Yy ◽  
Vena Cava ◽  
Diet Group ◽  
Vagal Afferents ◽  
Male Rats ◽  
Acid Oxidation ◽  
Peroxisome Proliferator ◽  
Gut Peptides ◽  
Nonesterified Fatty Acids

The endogenous lipid messenger oleoylethanolamide (OEA) inhibits eating and modulates fat metabolism supposedly through the activation of peroxisome proliferator-activated receptor-α (PPARα) and vagal sensory fibers. We tested in adult male rats whether OEA stimulates fatty acid oxidation (FAO) and ketogenesis and whether it increases plasma levels of the satiating gut peptides glucagon-like peptide-1 (GLP-1) and peptide YY (PYY). We also explored whether OEA still inhibits eating after subdiaphragmatic vagal deafferentation (SDA). We found that intraperitoneally injected OEA (10 mg/kg body wt) reduced ( P < 0.05) food intake mainly by increasing meal latency and that this effect was stronger in rats fed a 60% high-fat diet (HFD) than in chow-fed rats. OEA increased ( P < 0.05) postprandial plasma nonesterified fatty acids and β-hydroxybutyrate (BHB) in the hepatic portal vein (HPV) and vena cava (VC) 30 min after injection, which was more pronounced in HFD- than in chow-fed rats. OEA also increased the protein expression of the key ketogenetic enzyme, mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase, in the jejunum of HFD-fed rats, but not in the liver or duodenum of either diet group. Furthermore, OEA decreased GLP-1 and PYY concentrations ( P < 0.05) in the HPV and VC 30 min after administration. Finally, OEA reduced food intake in SDA and sham-operated rats similarly. Our findings indicate that neither intact abdominal vagal afferents nor prandial increases in GLP-1 or PYY are necessary for the satiety effect of OEA. The enhanced FAO and ketogenesis raise the possibility of an involvement of intestine-derived BHB in OEA's satiety effect under certain conditions.

Comparative effects of CCK-8 on feeding, sham feeding, and exocrine pancreatic secretion in rats

1986 ◽  
Vol 251 (1) ◽  
pp. R97-R105 ◽  
Author(s):  
R. D. Reidelberger ◽  
T. E. Solomon
Keyword(s):  
Food Intake ◽  
Pancreatic Secretion ◽  
Gastric Distension ◽  
Exocrine Pancreatic Secretion ◽  
Humoral Factors ◽  
Sham Feeding ◽  
Hormonal Mechanism ◽  
Satiety Hormone ◽  
Feeding Effect ◽  
Normal Feeding

Cholecystokinin (CCK) is thought to be a hormonal regulator of exocrine pancreatic secretion and is postulated to be a satiety hormone. We compared the dose-response effects of CCK octapeptide (CCK-8) on feeding, sham feeding, and pancreatic secretion to gauge whether the feeding effect might be physiological. Pancreatic responses to intravenous CCK-8 (40, 200, 1,000, or 4,000 pmol . kg-1 . h-1) in fasted unanesthetized rats were compared with effects of CCK-8 (0, 200, 1,000, or 4,000 pmol . kg-1 . h-1) on ingestion of liquid diet in fasted rats with gastric cannulas either closed (normal feeding) or open (sham feeding). Maximal pancreatic amylase output occurred at 200 pmol . kg-1 . h-1 of CCK-8; output declined at higher doses. Food intake was significantly inhibited only at 1,000 and 4,000 pmol . kg-1 . h-1 of CCK-8; the effect was similar when gastric cannulas were closed and open. These results, together with available data on the low postprandial levels of plasma CCK, suggest that circulating levels of CCK normally present after food intake are not sufficient to produce satiety. Furthermore, suppression of feeding by CCK does not appear to be mediated solely by a mechanism that senses gastric distension, because CCK-8 had similar effects in the presence and absence of gastric distension. Whether CCK interacts with other neural or humoral factors to produce satiety by a hormonal mechanism remains to be determined.

Blockade of type A, but not type B, CCK receptors postpones satiety in rhesus monkeys

1993 ◽  
Vol 265 (3) ◽  
pp. R620-R624 ◽  
Author(s):  
T. H. Moran ◽  
P. J. Ameglio ◽  
H. J. Peyton ◽  
G. J. Schwartz ◽  
P. R. McHugh
Keyword(s):  
Food Intake ◽  
Receptor Antagonist ◽  
Rhesus Monkeys ◽  
Type A ◽  
Intragastric Administration ◽  
Maximal Effect ◽  
Type B ◽  
Cck Receptors ◽  
Total Food Intake ◽  
Cck Receptor Antagonist

The exogenous administration of the brain/gut peptide cholecystokinin (CCK) inhibits food intake in a variety of species, including subhuman primates and humans. To determine the role of endogenously released CCK in the control of food intake in rhesus monkeys, we examined the ability of the selective type A and type B CCK antagonists devazepide and L-365260 to affect total daily food intake and various meal patterns. Various doses of the antagonists were administered intragastrically 30 min before a daily 4-h feeding period. One-gram food pellets were delivered in response to lever pulls, and intake was computer monitored. Intragastric administration of the type A CCK receptor antagonist devazepide (10-320 micrograms/kg) significantly increased food intake in a dose-related fashion. The threshold for increasing intake was 32 micrograms/kg, and a maximal effect was obtained at a dose of 100 micrograms/kg that increased total 4-h food intake by 47%. The effect of devazepide on food intake was mediated by significant increases in the size and duration of the initial meal, lengthening of the subsequent intermeal interval, and a decrease in the satiety ratio (intermeal interval/1st meal size). In contrast, intragastric administration of the type B CCK receptor antagonist L-365260 (3.2-320 micrograms/kg) did not significantly affect total food intake or any of the meal parameters. These data demonstrate that endogenously released CCK acting through type A CCK receptors plays a role in regulating food intake in rhesus monkeys.

scholarly journals Alterations in circadian and meal-induced gut peptide levels in lean and obese rats

2017 ◽  
Vol 242 (18) ◽  
pp. 1786-1794 ◽  
Author(s):  
Alexander A Moghadam ◽  
Timothy H Moran ◽  
Megan J Dailey
Keyword(s):  
Early Intervention ◽  
Food Intake ◽  
Glycemic Control ◽  
High Fat Diet ◽  
Peptide Yy ◽  
Light Cycle ◽  
Gut Peptides ◽  
High Fat ◽  
Metabolic Disturbances ◽  
Dark Cycle

Alterations in gut hormone signaling are a likely contributing factor to the metabolic disturbances associated with overweight/obesity as they coordinate the timing of feeding behavior, absorption, and utilization of nutrients. These hormones are released in response to food intake, or follow a circadian or anticipatory pattern of secretion that is independent of nutrient stimulation. The aim of this study was to identify the degree to which high-fat diet-induced obesity would alter the daily rhythm of gut peptide plasma levels (glucagon-like peptide-1 [GLP-1], peptide YY [PYY], insulin or amylin [AMY]) or meal-induced levels in the middle of the light or dark cycle. Male Sprague-Dawley rats were fed a high-fat diet (OBESE) or chow (LEAN), implanted with jugular catheters, and blood samples were taken every 2 h throughout the light/dark cycle while freely feeding or after an Ensure liquid meal. We found that even when OBESE and LEAN animals ate the same kcals and have a similar pattern of food intake, there is a difference in both the levels and rhythm of plasma gut peptides. GLP-1 and PYY are higher during the light cycle in LEAN animals and AMY is higher in the OBESE group throughout the light/dark cycle. There was also a differential response of plasma gut signals after the Ensure meal, even though the composition and amount of intake of the meal were the same in both groups. These changes occur prior to the high-fat diet induced loss of glycemic control and may be a target for early intervention. Impact statement The aim of this study was to test if obesity would alter the daily rhythm of gut peptides or meal-induced levels in the middle of the light or dark cycle. We found that even when animals are eating the same amount (in kcal) of food that the obese animals have altered daily rhythms and meal-induced gut peptide levels. In particular, we are the first to show that obesity induces increases in peptide YY levels during the light cycle and amylin remains high throughout the light and dark cycle in obese animals. These changes occurred prior to a loss of glycemic control. Thus, the rhythm of gut peptides could be used as an early indicator of later and more serious metabolic disturbances and may be a target for early intervention.

scholarly journals Peripheral and central mechanisms involved in the control of food intake by dietary amino acids and proteins

2012 ◽  
Vol 25 (1) ◽  
pp. 29-39 ◽  
Author(s):  
Gilles Fromentin ◽  
Nicolas Darcel ◽  
Catherine Chaumontet ◽  
Agnes Marsset-Baglieri ◽  
Nachiket Nadkarni ◽  
...  
Keyword(s):  
Food Intake ◽  
Arcuate Nucleus ◽  
Peptide Yy ◽  
Current Knowledge ◽  
Mammalian Target Of Rapamycin ◽  
Food Aversion ◽  
Gut Peptides ◽  
Principal Mechanism ◽  
Glucagon Like Peptide 1 ◽  
Diet Intake

The present review summarises current knowledge and recent findings on the modulation of appetite by dietary protein, via both peripheral and central mechanisms. Of the three macronutrients, proteins are recognised as the strongest inhibitor of food intake. The well-recognised poor palatability of proteins is not the principal mechanism explaining the decrease in high-protein (HP) diet intake. Consumption of a HP diet does not induce conditioned food aversion, but rather experience-enhanced satiety. Amino acid consumption is detected by multiple and redundant mechanisms originating from visceral (during digestion) and metabolic (inter-prandial period) sources, recorded both directly and indirectly (mainly vagus-mediated) by the central nervous system (CNS). Peripherally, the satiating effect of dietary proteins appears to be mediated by anorexigenic gut peptides, principally cholecystokinin, glucagon-like peptide-1 and peptide YY. In the CNS, HP diets trigger the activation of noradrenergic and adrenergic neurons in the nucleus of the solitary tract and melanocortin neurons in the arcuate nucleus. Additionally, there is evidence that circulating leucine levels may modulate food intake. Leucine is associated with neural mechanisms involving mammalian target of rapamycin (mTOR) and AMP-activated protein kinase (AMPK), energy sensors active in the control of energy intake, at least in the arcuate nucleus of the hypothalamus. In addition, HP diets inhibit the activation of opioid and GABAergic neurons in the nucleus accumbens, and thus inhibit food intake by reducing the hedonic response to food, presumably because of their low palatability. Future studies should concentrate on studying the adaptation of different neural circuits following the ingestion of protein diets.

scholarly journals Anorexigenic postprandial responses of PYY and GLP1 to slow ice cream consumption: preservation in obese adolescents, but not in obese adults

2013 ◽  
Vol 168 (3) ◽  
pp. 429-436 ◽  
Author(s):  
A E Rigamonti ◽  
F Agosti ◽  
E Compri ◽  
M Giunta ◽  
N Marazzi ◽  
...  
Keyword(s):  
Food Intake ◽  
Peptide Yy ◽  
Gut Hormones ◽  
Eating Rate ◽  
Gut Peptides ◽  
Physiological Control ◽  
Obese Adults ◽  
Obese Adolescent ◽  
Obese Adolescents ◽  
Circulating Levels

ObjectiveEating slowly increases the postprandial responses of some anorexigenic gut hormones in healthy lean subjects. As the rate of food intake is positively associated with obesity, the aim of the study was to determine whether eating the same meal at different rates evokes different postprandial anorexigenic responses in obese adolescent and adult subjects.Design and methodsEighteen obese adolescents and adults were enrolled. A test meal was consumed on two different sessions by each subject, meal duration taking either 5 min (fast feeding) or 30 min (slow feeding). Circulating levels of glucagon-like peptide 1 (GLP1), peptide YY (PYY), glucose, insulin, and triglycerides were measured over 210 min. Visual analog scales were used to evaluate the subjective feelings of hunger and satiety.ResultsFast feeding did not stimulate GLP1 release in obese adolescent and adults, whereas slow feeding increased circulating levels of GLP1 only in obese adolescents. Plasma PYY concentrations increased both in obese adolescents and in adults, irrespective of the eating rate, but slow feeding was more effective in stimulating PYY release in obese adolescents than in adults. Simultaneously, slow feeding evoked a higher satiety only in obese adolescents compared with fast feeding but not in obese adults. In obese adolescents, slow feeding decreased hunger (only at 210 min). Irrespective of the eating rate, postprandial responses of insulin and triglycerides were higher in obese adults than in obese adolescents. Conclusion: Slow feeding leads to higher concentrations of anorexigenic gut peptides and favors satiety in obese adolescents, but this physiological control of food intake is lost in obese adults.

scholarly journals Length and site of the small intestine exposed to fat influences hunger and food intake

2011 ◽  
Vol 106 (10) ◽  
pp. 1609-1615 ◽  
Author(s):  
P. W. Jeroen Maljaars ◽  
Harry P. F. Peters ◽  
Andrea Kodde ◽  
Maartje Geraedts ◽  
Fred J. Troost ◽  
...  
Keyword(s):  
Small Intestine ◽  
Food Intake ◽  
Peptide Yy ◽  
Control Treatment ◽  
Liquid Meal ◽  
Animal Data ◽  
Oral Control ◽  
Fat Infusion ◽  
Glucagon Like Peptide 1 ◽  
Experimental Treatments

The site of intestinal fat delivery affects satiety and may affect food intake in humans. Animal data suggest that the length of the small intestine exposed to fat is also relevant. The aim of the present study was to investigate whether increasing the areas of intestinal fat exposure and the way it is exposed would affect satiety parameters and food intake. In the present single-blind, randomised, cross-over study, fifteen volunteers, each intubated with a naso-ileal tube, received four treatments on consecutive days. The oral control (control treatment) was a liquid meal (LM) containing 6 g fat ingested att = 0 min, with saline infusion att = 30–120 min. Experimental treatments were a fat-free LM att = 0 min, with either 6 g oil delivered sequentially (2 g duodenal,t = 30–60 min; 2 g jejunal,t = 60–90 min; 2 g ileal,t = 90–120 min), simultaneously (2 g each to all sites,t = 30–120 min) or ileal only (6 g ileal,t = 30–120 min). Satiety parameters (hunger and fullness) and cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), peptide YY (PYY) secretion were measured untilt = 180 min, whenad libitumfood intake was assessed. Only the ileum treatment reduced food intake significantly over the control treatment. The ileum and simultaneous treatments significantly reduced hunger compared with the control treatment. Compared with control, no differences were observed for PYY, CCK and GLP-1 with regard to 180 min integrated secretion. Ileal fat infusion had the most pronounced effect on food intake and satiety. Increasing the areas of intestinal fat exposure only affected hunger when fat was delivered simultaneously, not sequentially, to the exposed areas. These results demonstrate that ileal brake activation offers an interesting target for the regulation of ingestive behaviour.

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