The role of the stomach in the control of appetite and the secretion of satiation peptides

2012 ◽  
Vol 302 (6) ◽  
pp. E666-E673 ◽  
Author(s):  
Robert E. Steinert ◽  
Anne C. Meyer-Gerspach ◽  
Christoph Beglinger
Keyword(s):  
Peptide Yy ◽  
Potential Interaction ◽  
Feedback Signal ◽  
Similar Degree ◽  
Short Term ◽  
Gastric Distention ◽  
Liquid Meal ◽  
Intraduodenal Infusion ◽  
Glucagon Like Peptide 1

It is widely accepted that gastric parameters such as gastric distention provide a direct negative feedback signal to inhibit eating; moreover, gastric and intestinal signals have been reported to synergize to promote satiation. However, there are few human data exploring the potential interaction effects of gastric and intestinal signals in the short-term control of appetite and the secretion of satiation peptides. We performed experiments in healthy subjects receiving either a rapid intragastric load or a continuous intraduodenal infusion of glucose or a mixed liquid meal. Intraduodenal infusions (3 kcal/min) were at rates comparable with the duodenal delivery of these nutrients under physiological conditions. Intraduodenal infusions of glucose elicited only weak effects on appetite and the secretion of glucagon-like peptide-1 (GLP-1) and peptide YY (PYY). In contrast, identical amounts of glucose delivered intragastrically markedly suppressed appetite ( P < 0.05) paralleled by greatly increased plasma levels of GLP-1 and PYY (≤3-fold, P < 0.05). Administration of the mixed liquid meal showed a comparable phenomenon. In contrast to GLP-1 and PYY, plasma ghrelin was suppressed to a similar degree with both intragastric and intraduodenal nutrients. Our data confirm that the stomach is an important element in the short-term control of appetite and suggest that gastric and intestinal signals interact to mediate early fullness and satiation potentially by increased GLP-1 and PYY secretions.

Comparative effects of intraduodenal protein and lipid on ghrelin, peptide YY, and leptin release in healthy men

2015 ◽  
Vol 308 (4) ◽  
pp. R300-R304 ◽  
Author(s):  
Sina S. Ullrich ◽  
Bärbel Otto ◽  
Amy T. Hutchison ◽  
Natalie D. Luscombe-Marsh ◽  
Michael Horowitz ◽  
...  
Keyword(s):  
Energy Intake ◽  
Peptide Yy ◽  
Saline Control ◽  
Short Term ◽  
Intraduodenal Infusion ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Underlying Mechanisms ◽  
Plasma Leptin

Intraduodenal infusion of lipid or protein potently reduces subsequent energy intake. There is evidence that the underlying mechanisms differ significantly between the two nutrients. While intraduodenal lipid stimulates glucagon-like peptide-1 and CCK much more than protein, the release of insulin and glucagon is substantially greater in response to protein. Ghrelin and PYY are both involved in short-term regulation, while leptin is a long-term regulator, of energy balance; the acute effects of nutrients on leptin release are unclear. We investigated the comparative effects of intraduodenal lipid and protein on plasma ghrelin, PYY, and leptin concentrations. Thirteen lean, young men received 90-min intraduodenal infusions of protein (whey hydrolysate) or lipid (long-chain triglyceride emulsion) at a rate of 3 kcal/min, or saline control, on three separate days. Blood samples were collected at baseline and regularly during infusions. Both lipid and protein potently suppressed plasma ghrelin compared with control (both P < 0.001), with no difference between them. While both lipid and protein stimulated plasma PYY ( P < 0.001), the effect of lipid was substantially greater than that of protein ( P < 0.001). Neither intraduodenal lipid nor protein affected plasma leptin. In conclusion, intraduodenal lipid and protein have discrepant effects on the release of PYY, but not ghrelin. When considered with our previous findings, it appears that, with the exception of ghrelin, the energy intake-suppressant effects of lipid and protein are mediated by different mechanisms.

scholarly journals Ileal short-chain fatty acids inhibit gastric motility by a humoral pathway

2000 ◽  
Vol 279 (5) ◽  
pp. G925-G930 ◽  
Author(s):  
G. Cuche ◽  
J. C. Cuber ◽  
C. H. Malbert
Keyword(s):  
Gastric Motility ◽  
Short Chain Fatty Acid ◽  
Peptide Yy ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
Maximal Amplitude ◽  
Inhibiting Factor ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

The aim of this study was to evaluate the nervous and humoral pathways involved in short-chain fatty acid (SCFA)-induced ileal brake in conscious pigs. The role of extrinsic ileal innervation was evaluated after SCFA infusion in innervated and denervated Babkin's ileal loops, and gastric motility was measured with strain gauges. Peptide YY (PYY) and glucagon-like peptide-1 (GLP-1) concentrations were evaluated in both situations. The possible involvement of absorbed SCFA was tested by using intravenous infusion of acetate. Ileal SCFA infusion in the intact terminal ileum decreased the amplitude of distal and terminal antral contractions (33 ± 1.2 vs. 49 ± 1.2% of the maximal amplitude recorded before infusion) and increased their frequency (1.5 ± 0.11 vs. 1.3 ± 0.10/min). Similar effects were observed during SCFA infusion in ileal innervated and denervated loops (amplitude, 35 ± 1.0 and 34 ± 0.8 vs. 47 ± 1.3 and 43 ± 1.2%; frequency, 1.4 ± 0.07 and 1.6 ± 0.06 vs. 1.1 ± 0.14 and 1.0 ± 0.12/min). Intravenous acetate did not modify the amplitude and frequency of antral contractions. PYY but not GLP-1 concentrations were increased during SCFA infusion in innervated and denervated loops. In conclusion, ileal SCFA inhibit distal gastric motility by a humoral pathway involving the release of an inhibiting factor, which is likely PYY.

Effects of omega fatty acids on the short-term postprandial satiety related peptides in rats

2022 ◽  
Author(s):  
Hilal Hizli Guldemir ◽  
Nihal Buyukuslu ◽  
Pakize Yigit ◽  
Cagri Cakici ◽  
Ekrem Musa Ozdemir
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Peptide Yy ◽  
Insulin Response ◽  
Omega Fatty Acids ◽  
Oral Gavage ◽  
Short Term ◽  
Adult Rats ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Abstract. We aimed to assess the effects of omega fatty acids on time depending on responses of satiety hormones. Sixty adult rats were randomly divided into 4 groups; linoleic acid (LA), α-linolenic acid (ALA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) groups. For each fatty acid, the dose of 400 mg/kg was applied by oral gavage. Blood samples were taken after the 15, 30, 60 and 120 minutes. Ghrelin, cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), peptide YY (PYY), leptin and insulin hormones were analyzed by ELISA. We observed the significant increases (p<0.05) of the levels of CCK between n-3 (ALA, at 60th min; EPA, at 30th and 60th min and DHA, at 60 min) and n-6 (LA) supplemented rats. The highest GLP-1 levels were in ALA (0.70 ng/mL) and DHA (0.67 ng/mL) supplemented groups at 60th and 120th min indicating n-3 fatty acids efficiency on satiety compared to LA. It seems that ALA at 60th min and EPA at 120th min could provide the highest satiety effect with the highest insulin response, while the efficiency of LA supplementation on insulin-induced satiety diminished. The only significant change in AUC values among all hormones was in the CCK of the ALA group (p=0.004). The level of leptin increased in DHA and EPA supplemented rats (p=0.140). Our results showed that dietary omega fatty acids influenced the releasing of hormones in different ways possibly depending on chain length or saturation degree. Comprehensive studies need to be addressed for each fatty acid on satiety-related peptide hormones.

scholarly journals The Role of the Vagal Nerve in Peripheral PYY3–36-Induced Feeding Reduction in Rats

Endocrinology ◽  
2005 ◽  
Vol 146 (5) ◽  
pp. 2369-2375 ◽  
Author(s):  
Shuichi Koda ◽  
Yukari Date ◽  
Noboru Murakami ◽  
Takuya Shimbara ◽  
Takeshi Hanada ◽  
...  
Keyword(s):  
Peptide Yy ◽  
Gastrointestinal Hormones ◽  
Blood Stream ◽  
Afferent Nerve ◽  
Solitary Tract ◽  
Afferent Fibers ◽  
Vagal Afferent ◽  
Glucagon Like Peptide 1 ◽  
The Brain

Abstract Peptide YY (PYY), an anorectic peptide, is secreted postprandially from the distal gastrointestinal tract. PYY3–36, the major form of circulating PYY, binds to the hypothalamic neuropeptide Y Y2 receptor (Y2-R) with a high-affinity, reducing food intake in rodents and humans. Additional gastrointestinal hormones involved in feeding, including cholecystokinin, glucagon-like peptide 1, and ghrelin, transmit satiety or hunger signals to the brain via the vagal afferent nerve and/or the blood stream. Here we determined the role of the afferent vagus nerve in PYY function. Abdominal vagotomy abolished the anorectic effect of PYY3–36 in rats. Peripheral administration of PYY3–36 induced Fos expression in the arcuate nucleus of sham-operated rats but not vagotomized rats. We showed that Y2-R is synthesized in the rat nodose ganglion and transported to the vagal afferent terminals. PYY3–36 stimulated firing of the gastric vagal afferent nerve when administered iv. Considering that Y2-R is present in the vagal afferent fibers, PYY3–36 could directly alter the firing rate of the vagal afferent nerve via Y2-R. We also investigated the effect of ascending fibers from the nucleus of the solitary tract on the transmission of PYY3–36-mediated satiety signals. In rats, bilateral midbrain transections rostral to the nucleus of the solitary tract also abolished PYY3–36-induced reductions in feeding. This study indicates that peripheral PYY3–36 may transmit satiety signals to the brain in part via the vagal afferent pathway.

scholarly journals Short-term treatment with olanzapine does not modulate gut hormone secretion: olanzapine disintegrating versus standard tablets

2010 ◽  
Vol 162 (1) ◽  
pp. 75-83 ◽  
Author(s):  
Solrun Vidarsdottir ◽  
Ferdinand Roelfsema ◽  
Trea Streefland ◽  
Jens J Holst ◽  
Jens F Rehfeld ◽  
...  
Keyword(s):  
Weight Gain ◽  
Peptide Yy ◽  
Hormone Secretion ◽  
Gut Hormones ◽  
Term Treatment ◽  
Short Term ◽  
Short Term Treatment ◽  
Healthy Men ◽  
Gut Hormone ◽  
Glucagon Like Peptide 1

BackgroundTreatment with olanzapine (atypical antipsychotic drug) is frequently associated with various metabolic anomalies, including obesity, dyslipidemia, and diabetes mellitus. Recent data suggest that olanzapine orally disintegrating tablets (ODT), which dissolve instantaneously in the mouth, might cause less weight gain than olanzapine standard oral tablets (OST).Design and methodsTen healthy men received olanzapine ODT (10 mg o.d., 8 days), olanzapine OST (10 mg o.d., 8 days), or no intervention in a randomized crossover design. At breakfast and dinner, blood samples were taken for measurement of pancreatic polypeptide, peptide YY, glucagon-like peptide-1, total glucagon, total ghrelin, and cholecystokinin (CCK) concentrations.ResultsWith the exception of pre- and postprandial concentration of ghrelin at dinner and preprandial CCK concentrations at breakfast, which were all slightly increased (respectivelyP=0.048,P=0.034 andP=0.042), olanzapine did not affect gut hormone concentrations. Thus, olanzapine ODT and OST had similar effects on gut hormone secretion.ConclusionShort-term treatment with olanzapine does not have major impact on the plasma concentration of gut hormones we measured in healthy men. Moreover, despite pharmacological difference, gut hormone concentrations are similar during treatment with olanzapine ODT and OST. The capacity of olanzapine to induce weight gain and diabetes is unlikely to be caused by modulation of the secretion of gut hormones measured here. We cannot exclude the possibility that olanzapine's impact on other gut hormones, to impair insulin sensitivity and stimulate weight gain, exists.

scholarly journals Current and emerging concepts on the role of peripheral signals in the control of food intake and development of obesity

2012 ◽  
Vol 108 (5) ◽  
pp. 778-793 ◽  
Author(s):  
F. A. Duca ◽  
M. Covasa
Keyword(s):  
Body Weight ◽  
Energy Homeostasis ◽  
Peptide Yy ◽  
Body Weight Gain ◽  
Gut Peptides ◽  
Gastrointestinal Peptides ◽  
Term Energy ◽  
Glucagon Like Peptide 1 ◽  
Treatment Of Obesity

The gastrointestinal peptides are classically known as short-term signals, primarily inducing satiation and/or satiety. However, accumulating evidence has broadened this view, and their role in long-term energy homeostasis and the development of obesity has been increasingly recognised. In the present review, the recent research involving the role of satiation signals, especially ghrelin, cholecystokinin, glucagon-like peptide 1 and peptide YY, in the development and treatment of obesity will be discussed. Their activity, interactions and release profile vary constantly with changes in dietary and energy influences, intestinal luminal environment, body weight and metabolic status. Manipulation of gut peptides and nutrient sensors in the oral and postoral compartments through diet and/or changes in gut microflora or using multi-hormone ‘cocktail’ therapy are among promising approaches aimed at reducing excess food consumption and body-weight gain.

scholarly journals Role of Guanylate kinase 1 in SARS CoV-2 Replication and tumorigenesis: Potential Role for Amantadine and Novel Therapeutics in COVID-19 and Cancer Management.

2021 ◽  
Author(s):  
Mina Kelleni
Keyword(s):  
Crucial Role ◽  
Potential Role ◽  
Swot Analysis ◽  
Physiological Function ◽  
Potential Interaction ◽  
Short Term ◽  
Guanylate Kinase ◽  
Cancer Management

A recent study has suggested that guanylate kinase 1 (GK1) plays a crucial role in SARS CoV-2 replication and recommended to test GK 1 inhibitors for invitro experiments and previous studies have suggested a role in the pathogenesis of some neoplasms. We are providing a concise strengths, weaknesses, opportunities, and threats (SWOT) analysis of this hypothesis while discussing guanylate kinase physiological function, pharmacological importance. Importantly, we suggest assessing another potential interaction between SARS CoV-2 and the non-authentic membrane-associated guanylate kinases as we suggest this might add to consider the potential role of amantadine in COVID-19 management. Moreover, though GK1 role in SARS CoV-2 replication might prove valid, the available experimental inhibitors of GK 1 might not, at least for the short term, be safely used to manage COVID-19. Finally, we recommend conducting genetic, physiological, and immunological studies to explore the long-term potentials of GK-1 inhibitors suggesting they might eventually lead to a novel COVID-19 and cancer pharmacotherapeutics.

scholarly journals Intestinal NAPE-PLD contributes to short-term regulation of food intake via gut-to-brain axis

2020 ◽  
Vol 319 (3) ◽  
pp. E647-E657
Author(s):  
Marialetizia Rastelli ◽  
Matthias Van Hul ◽  
Romano Terrasi ◽  
Charlotte Lefort ◽  
Marion Régnier ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Physiological Role ◽  
Intestinal Epithelial ◽  
Wild Type ◽  
Short Term ◽  
Physiological Mechanisms ◽  
Short Term Exposure ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Our objective was to explore the physiological role of the intestinal endocannabinoids in the regulation of appetite upon short-term exposure to high-fat-diet (HFD) and understand the mechanisms responsible for aberrant gut-brain signaling leading to hyperphagia in mice lacking Napepld in the intestinal epithelial cells (IECs). We generated a murine model harboring an inducible NAPE-PLD deletion in IECs ( NapepldΔIEC). After an overnight fast, we exposed wild-type (WT) and NapepldΔIEC mice to different forms of lipid challenge (HFD or gavage), and we compared the modification occurring in the hypothalamus, in the vagus nerve, and at endocrine level 30 and 60 min after the stimulation. NapepldΔIEC mice displayed lower hypothalamic levels of N-oleoylethanolamine (OEA) in response to HFD. Lower mRNA expression of anorexigenic Pomc occurred in the hypothalamus of NapepldΔIEC mice after lipid challenge. This early hypothalamic alteration was not the consequence of impaired vagal signaling in NapepldΔIEC mice. Following lipid administration, WT and NapepldΔIEC mice had similar portal levels of glucagon-like peptide-1 (GLP-1) and similar rates of GLP-1 inactivation. Administration of exendin-4, a full agonist of GLP-1 receptor (GLP-1R), prevented the hyperphagia of NapepldΔIEC mice upon HFD. We conclude that in response to lipid, NapepldΔIEC mice displayed reduced OEA in brain and intestine, suggesting an impairment of the gut-brain axis in this model. We speculated that decreased levels of OEA likely contributes to reduce GLP-1R activation, explaining the observed hyperphagia in this model. Altogether, we elucidated novel physiological mechanisms regarding the gut-brain axis by which intestinal NAPE-PLD regulates appetite rapidly after lipid exposure.

Sign in / Sign up

Export Citation Format

Share Document