Effect of pancreatic polypeptide on gastric accommodation and gastric emptying in conscious rats

2014 ◽  
Vol 307 (1) ◽  
pp. G122-G128 ◽  
Author(s):  
Sofie Verschueren ◽  
Pieter Janssen ◽  
Lukas Van Oudenhove ◽  
Leif Hultin ◽  
Jan Tack
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Pancreatic Polypeptide ◽  
Gastric Fistula ◽  
X Rays ◽  
Gastric Accommodation ◽  
Nitric Oxide Release ◽  
F Cells ◽  
Vehicle Treatment ◽  
Nutrient Infusion

Pancreatic polypeptide (PP) is an anorexigenic hormone released from pancreatic F cells upon food intake. We aimed to determine the effect of PP on gastric accommodation and gastric emptying in conscious Wistar HAN rats to investigate whether effects on motor function could contribute to its anorexigenic effects. Intragastric pressure (IGP) was measured through a chronically implanted gastric fistula during the infusion of a nutrient meal (Nutridrink; 0.5 ml/min). Rats were treated with PP (0, 33 and 100 pmol·kg−1·min−1) in combination with NG-nitro-l-arginine methyl ester (l-NAME; 180 mg·kg−1·h−1), atropine (3 mg·kg−1·h−1), or vehicle. Furthermore, the effect of PP was tested after subdiaphragmal vagotomy of the stomach. Gastric emptying of a noncaloric and a caloric meal after treatment with 100 pmol·kg−1·min−1PP or vehicle was compared using X-rays. PP significantly increased IGP during nutrient infusion compared with vehicle ( P < 0.01). l-NAME and atropine significantly increased IGP during nutrient infusion compared with vehicle treatment ( P < 0.005 and 0.01, respectively). The effect of PP on IGP during nutrient infusion was abolished in the presence of l-NAME and in the presence of atropine. In vagotomized rats, PP increased IGP compared with intact controls ( P < 0.05). PP significantly delayed gastric emptying of both a noncaloric ( P < 0.05) and a caloric ( P < 0.005) meal. PP inhibits gastric accommodation and delays gastric emptying, probably through inhibition of nitric oxide release. These results indicate that, besides the well-known centrally mediated effects, PP might decrease food intake through peripheral mechanisms.

Effects of bombesin on food intake and gastric acid secretion in cats

1989 ◽  
Vol 256 (1) ◽  
pp. R181-R186
Author(s):  
A. Bado ◽  
M. J. Lewin ◽  
M. Dubrasquet
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Gastric Secretion ◽  
Acid Secretion ◽  
Gastric Fistula ◽  
Single Class ◽  
Heidenhain Pouch ◽  
Daily Food Intake ◽  
Feeding Experiments ◽  
Daily Food

The brain and gut peptide bombesin has been reported both to stimulate gastric secretion and to induce satiety. To understand how the peripheral administration of bombesin affects food intake and whether gastric mechanisms are involved, a comparative study of the doses of bombesin active on gastric secretion, gastric emptying, and food intake was undertaken in cats provided with a gastric fistula and a denervated Heidenhain pouch. The smallest dose of intravenous bombesin that stimulated significantly basal acid secretion (20 pmol.kg-1.h-1) by the gastric fistula also enhanced meal-stimulated acid secretion by the Heidenhain pouch (+138%, P less than 0.01), delayed gastric emptying of a liquid protein meal (-30%, P less than 0.01), and suppressed food intake when the test meal was allowed to reach the stomach (-15%, P less than 0.01). Conversely, in sham-feeding experiments, the same dose of bombesin increased food intake (+35%, P less than 0.01). In full-day experiments conducted in nonfasted cats, bombesin decreased both the food intake in the 4-h period after the infusion and the daily food intake, whereas octapeptide cholecystokinin induced a transient satiety but did not decrease daily food intake. These results indicate that in cats the interaction of bombesin with "pregastric" mechanisms is not sufficient to induce satiety and that a relation could exist between the effects of bombesin on gastric secretion, emptying, and food intake. A single class of receptors might be involved in these peripheral effects of bombesin.

scholarly journals The Effect of Pancreatic Polypeptide on Gastric Emptying, Gastric Accommodation and Satiation in Healthy Volunteers

2011 ◽  
Vol 140 (5) ◽  
pp. S-305
Author(s):  
Sofie Verschueren ◽  
Pieter Janssen ◽  
Rita Vos ◽  
Kristin Verbeke ◽  
Jan F. Tack
Keyword(s):  
Gastric Emptying ◽  
Healthy Volunteers ◽  
Pancreatic Polypeptide ◽  
Gastric Accommodation

scholarly journals Gastric Sensory and Motor Functions and Energy Intake in Health and Obesity—Therapeutic Implications

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1158
Author(s):  
Lizeth Cifuentes ◽  
Michael Camilleri ◽  
Andres Acosta
Keyword(s):  
Energy Consumption ◽  
Gastric Emptying ◽  
Food Intake ◽  
Gastric Volume ◽  
Obesity Management ◽  
Bariatric Endoscopy ◽  
Motor Functions ◽  
Therapeutic Implications ◽  
Intestinal Functions

Sensory and motor functions of the stomach, including gastric emptying and accommodation, have significant effects on energy consumption and appetite. Obesity is characterized by energy imbalance; altered gastric functions, such as rapid gastric emptying and large fasting gastric volume in obesity, may result in increased food intake prior to reaching usual fullness and increased appetite. Thus, many different interventions for obesity, including different diets, anti-obesity medications, bariatric endoscopy, and surgery, alter gastric functions and gastrointestinal motility. In this review, we focus on the role of the gastric and intestinal functions in food intake, pathophysiology of obesity, and obesity management.

scholarly journals GLP-2 receptor in POMC neurons suppresses feeding behavior and gastric motility

2012 ◽  
Vol 303 (7) ◽  
pp. E853-E864 ◽  
Author(s):  
Xinfu Guan ◽  
Xuemei Shi ◽  
Xiaojie Li ◽  
Benny Chang ◽  
Yi Wang ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Feeding Behavior ◽  
Gastric Motility ◽  
Late Onset ◽  
Physiological Role ◽  
Immune Defense ◽  
Melanocortin Receptor ◽  
Melanocortin System ◽  
Dorsomedial Nucleus

Glucagon-like peptides (GLP-1/2) are cosecreted from endocrine L cells in the gut and preproglucagonergic neurons in the brain. Peripheral GLP-2 action is essential for maintaining intestinal homeostasis, improving absorption efficiency and blood flow, promoting immune defense, and producing efficacy in treatment of gastrointestinal diseases. However, it is unknown if CNS GLP-2 plays a physiological role in the control of energy homeostasis. Since GLP-1/2 are cotranslated from preproglucagongene and coproduced by prohormone convertase-1, it is challenging to knockout GLP-2 only. Instead, our laboratory has generated a Glp2r-floxed mouse line to dissect cell-specific GLP-2 receptor GLP-2R) action in the regulation of energy balance. Our objective was to determine if GLP-2R in the hypothalamus modulates feeding behavior and gastric emptying. We show that Glp2r mRNA and protein are highly expressed in the arcuate nucleus and dorsomedial nucleus of the mouse hypothalamus. Using the Cre-LoxP system, we generated mice that lack Glp2r expression in POMC neurons (KO; mainly in the hypothalamus). The KO mice showed hyperphagic behavior (such as increases in food intake and meal frequency), accelerated gastric emptying (assessed by [13C]octanoic acid breath test), and late-onset obesity, yet there was no decrease in basal metabolic rate. Infusion of GLP-2 (2.5 nmol into the 4th ventricle) suppressed food intake and gastric emptying, while GLP-2-mediated effects were abolished in the melanocortin receptor-4 (MC4R) KO mice. We conclude that Glp2r deletion in POMC neurons enhances feeding behavior and gastric motility, whereas icv GLP-2R activation suppresses food intake and gastric emptying through the MC4R signaling pathway. This study indicates that CNS GLP-2R plays a physiological role in the control of feeding behavior and gastric emptying and that this is mediated probably through the melanocortin system.

Relationship between Gastric Emptying or Gastric Accommodation and Postprandial Symptoms Observed After Ingestion of a Maximum Volume of a Nutrient Drink in 285 Participants

2017 ◽  
Vol 152 (5) ◽  
pp. S932-S933 ◽  
Author(s):  
Houssam Halawi ◽  
Alan R. Zinsmeister ◽  
Andres J. Acosta Cardenas ◽  
Maria Vazquez Roque ◽  
Ibironke Oduyebo ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Maximum Volume ◽  
Gastric Accommodation

LPS inhibits fasted plasma ghrelin levels in rats: role of IL-1 and PGs and functional implications

2006 ◽  
Vol 291 (4) ◽  
pp. G611-G620 ◽  
Author(s):  
Lixin Wang ◽  
Nicole R. Basa ◽  
Almaas Shaikh ◽  
Andrew Luckey ◽  
David Heber ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Gastric Emptying ◽  
Food Intake ◽  
Intravenous Injection ◽  
Plasma Levels ◽  
Inhibitory Action ◽  
Functional Implications ◽  
Urocortin 1 ◽  
Fasted Rats

LPS injected intraperitoneally decreases fasted plasma levels of ghrelin at 3 h postinjection in rats. We characterized the inhibitory action of LPS on plasma ghrelin and whether exogenous ghrelin restores LPS-induced suppression of food intake and gastric emptying in fasted rats. Plasma ghrelin and insulin and blood glucose were measured after intraperitoneal injection of LPS, intravenous injection of IL-1β and urocortin 1, and in response to LPS under conditions of blockade of IL-1 or CRF receptors by subcutaneous injection of IL-1 receptor antagonist (IL-1Ra) or astressin B, respectively, and prostaglandin (PG) synthesis by intraperitoneal indomethacin. Food intake and gastric emptying were measured after intravenous injection of ghrelin at 5 h postintraperitoneal LPS injection. LPS inhibited the elevated fasted plasma ghrelin levels by 47.6 ± 4.9%, 58.9 ± 3.3%, 74.4 ± 2.7%, and 48.9 ± 8.7% at 2, 3, 5, and 7 h postinjection, respectively, and values returned to preinjection levels at 24 h. Insulin levels were negatively correlated to those of ghrelin, whereas there was no significant correlation between glucose and ghrelin. IL-1Ra and indomethacin prevented the first 3-h decline in ghrelin levels induced by LPS, whereas astressin B did not. IL-1β inhibited plasma ghrelin levels, whereas urocortin 1 had no influence. Ghrelin injected intravenously prevented an LPS-induced 87% reduction of gastric emptying and 61% reduction of food intake. These data showed that IL-1 and PG pathways are part of the early mechanisms by which LPS suppresses fasted plasma ghrelin and that exogenous ghrelin can normalize LPS-induced-altered digestive functions.

Beaumont's Contribution to Gastric Psychophysiology: A Reappraisal

1988 ◽  
Vol 33 (7) ◽  
pp. 650-653 ◽  
Author(s):  
François M. Mai
Keyword(s):  
Gastric Emptying ◽  
Delayed Gastric Emptying ◽  
Bile Reflux ◽  
Emotional Arousal ◽  
Gastric Fistula ◽  
Physiological Changes ◽  
Digestive Process ◽  
Psychophysiological Research ◽  
Series Of Experiments

William Beaumont's monograph on the physiology of digestion which was first published in 1833, has become a classic in its field. In a series of experiments over a 10 year period on Alexis St. Martin, a 19 year old Canadian voyageur with a traumatic gastric fistula, Beaumont was the first to describe many important aspects of the digestive process. In two of the 238 experiments Beaumont noted gastric physiological changes induced by emotional arousal, these being bile reflux and delayed gastric emptying. Elsewhere in the book, but not in experimental context, Beaumont referred to non-specific changes in coloration and secretion of the mucous membrane induced by emotion. Modern gastric psychophysiological research has shown that emotional arousal increases, and withdrawal decreases, gastric acid secretion. It has also been shown conclusively that emotion can cause a reflux of bile into the stomach and it may delay gastric emptying. Although the main thrust of Beaumont's work was physiological, he must be credited with being the first investigator to draw attention to the role of emotional arousal in the digestive process.

Sign in / Sign up

Export Citation Format

Share Document