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 ◽  
...  

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.

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1104
Author(s):  
Cong Xie ◽  
Weikun Huang ◽  
Richard L. Young ◽  
Karen L. Jones ◽  
Michael Horowitz ◽  
...  

Bile acids are cholesterol-derived metabolites with a well-established role in the digestion and absorption of dietary fat. More recently, the discovery of bile acids as natural ligands for the nuclear farnesoid X receptor (FXR) and membrane Takeda G-protein-coupled receptor 5 (TGR5), and the recognition of the effects of FXR and TGR5 signaling have led to a paradigm shift in knowledge regarding bile acid physiology and metabolic health. Bile acids are now recognized as signaling molecules that orchestrate blood glucose, lipid and energy metabolism. Changes in FXR and/or TGR5 signaling modulates the secretion of gastrointestinal hormones including glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), hepatic gluconeogenesis, glycogen synthesis, energy expenditure, and the composition of the gut microbiome. These effects may contribute to the metabolic benefits of bile acid sequestrants, metformin, and bariatric surgery. This review focuses on the role of bile acids in energy intake and body weight, particularly their effects on gastrointestinal hormone secretion, the changes in obesity and T2D, and their potential relevance to the management of metabolic disorders.


2000 ◽  
Vol 279 (5) ◽  
pp. G925-G930 ◽  
Author(s):  
G. Cuche ◽  
J. C. Cuber ◽  
C. H. Malbert

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.


Nutrients ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 157 ◽  
Author(s):  
Marta Klementova ◽  
Lenka Thieme ◽  
Martin Haluzik ◽  
Renata Pavlovicova ◽  
Martin Hill ◽  
...  

Gastrointestinal hormones are involved in regulation of glucose metabolism and satiety. We tested the acute effect of meal composition on these hormones in three population groups. A randomized crossover design was used to examine the effects of two energy- and macronutrient-matched meals: a processed-meat and cheese (M-meal) and a vegan meal with tofu (V-meal) on gastrointestinal hormones, and satiety in men with type 2 diabetes (T2D, n = 20), obese men (O, n = 20), and healthy men (H, n = 20). Plasma concentrations of glucagon-like peptide -1 (GLP-1), amylin, and peptide YY (PYY) were determined at 0, 30, 60, 120 and 180 min. Visual analogue scale was used to assess satiety. We used repeated-measures Analysis of variance (ANOVA) for statistical analysis. Postprandial secretion of GLP-1 increased after the V-meal in T2D (by 30.5%; 95%CI 21.2 to 40.7%; p < 0.001) and H (by 15.8%; 95%CI 8.6 to 23.5%; p = 0.01). Postprandial plasma concentrations of amylin increased in in all groups after the V-meal: by 15.7% in T2D (95%CI 11.8 to 19.6%; p < 0.001); by 11.5% in O (95%CI 7.8 to 15.3%; p = 0.03); and by 13.8% in H (95%CI 8.4 to 19.5%; p < 0.001). An increase in postprandial values of PYY after the V-meal was significant only in H (by 18.9%; 95%CI 7.5 to 31.3%; p = 0.03). Satiety was greater in all participants after the V-meal: by 9% in T2D (95%CI 4.4 to 13.6%; p = 0.004); by 18.7% in O (95%CI 12.8 to 24.6%; p < 0.001); and by 25% in H (95%CI 18.2 to 31.7%; p < 0.001). Our results indicate there is an increase in gut hormones and satiety, following consumption of a single plant-based meal with tofu when compared with an energy- and macronutrient-matched processed-meat meat and cheese meal, in healthy, obese and diabetic men.


2011 ◽  
Vol 301 (5) ◽  
pp. R1479-R1485 ◽  
Author(s):  
Matthew R. Hayes ◽  
Scott E. Kanoski ◽  
Bart C. De Jonghe ◽  
Theresa M. Leichner ◽  
Amber L. Alhadeff ◽  
...  

The incretin and food intake suppressive effects of intraperitoneally administered glucagon-like peptide-1 (GLP-1) involve activation of GLP-1 receptors (GLP-1R) expressed on vagal afferent fiber terminals. Central nervous system processing of GLP-1R-driven vagal afferents results in satiation signaling and enhanced insulin secretion from pancreatic-projecting vagal efferents. As the vast majority of endogenous GLP-1 is released from intestinal l-cells following ingestion, it stands to reason that paracrine GLP-1 signaling, activating adjacent GLP-1R expressed on vagal afferent fibers of gastrointestinal origin, contributes to glycemic and food intake control. However, systemic GLP-1R-mediated control of glycemia is currently attributed to endocrine action involving GLP-1R expressed in the hepatoportal bed on terminals of the common hepatic branch of the vagus (CHB). Here, we examine the hypothesis that activation of GLP-1R expressed on the CHB is not required for GLP-1's glycemic and intake suppressive effects, but rather paracrine signaling on non-CHB vagal afferents is required to mediate GLP-1's effects. Selective CHB ablation (CHBX), complete subdiaphragmatic vagal deafferentation (SDA), and surgical control rats received an oral glucose tolerance test (2.0 g glucose/kg) 10 min after an intraperitoneal injection of the GLP-1R antagonist, exendin-(9–39) (Ex-9; 0.5 mg/kg) or vehicle. CHBX and control rats showed comparable increases in blood glucose following blockade of GLP-1R by Ex-9, whereas SDA rats failed to show a GLP-1R-mediated incretin response. Furthermore, GLP-1(7–36) (0.5 mg/kg ip) produced a comparable suppression of 1-h 25% glucose intake in both CHBX and control rats, whereas intake suppression in SDA rats was blunted. These findings support the hypothesis that systemic GLP-1R mediation of glycemic control and food intake suppression involves paracrine-like signaling on GLP-1R expressed on vagal afferent fibers of gastrointestinal origin but does not require the CHB.


1989 ◽  
Vol 13 ◽  
pp. 7-26 ◽  
Author(s):  
J. M. Forbes ◽  
J. E. Blundell

AbstractThe central nervous system is the integrator of most of the actions of the animal and as such plays a vital rôle in the control of voluntary food intake. Much of the work to understand how intake is controlled has been carried out with rats but that which has been done with pigs is included. The first experiments used electrolytic lesions in the designation of the ‘hunger centre’ and the ‘satiety centre’. Recent work has identified the paraventricular nucleus as a sensing site for experimental manipulations. Chemical stimulation of the brain has also been carried out to try to gain understanding of the rôle of neurotransmitters. Noradrenaline (NA) stimulates intake when given into many sites. Serotonin (5-HT) inhibits intake and has been claimed to play a rôle in the selection of macronutrients but 5-HT must now be interpreted in the light of the existence of several different subtypes of 5-HT receptors. Dopamine appears to moderate the hedonic response of eating. Numerous peptides are active in the brain where their rôle as neuromodulators may be quite different from their function in the periphery and at least three types of opioid receptors are implicated with kappa antagonists producing the most potent facilitatory effects. Neuropeptide Y and peptide YY produce massive orexigenic effects which readily overcome peripheral satiety factors. The brain cannot control intake in isolation. It receives inputs in the blood stream, such as glucose, as well as via the nervous system, both from the special senses and from visceral organs such as stomach, intestines and liver. Taste and olfaction are important in diet selection and a specific appetite for protein has been demonstrated in the pig.


2019 ◽  
Vol 26 (3) ◽  
pp. 280-292 ◽  
Author(s):  
Raoul Pop ◽  
Seong-Ho Kong ◽  
Allan Langlois ◽  
Francesco Marchegiani ◽  
Eran Shlomovitz ◽  
...  

Purpose. Targeted embolization of gastrointestinal (GI) arteries can modify hormonal production. We aimed to evaluate the impact of the embolization of the gastroduodenal artery (GDA) on the activity of foregut mucosa. Methods. The GDA’s duodenal branch was embolized in 12 Yucatan pigs using 100-300 µm (group A; n = 4) or 300-500 µm (group B; n = 4) microspheres, followed by coiling of the branch. In 4 animals (sham), only saline was injected. The levels of GI hormones (ghrelin, glucose-dependent insulinotropic peptide [GIP], glucagon-like peptide-1 [GLP-1], insulin, peptide YY [PYY], leptin) and the gene expression of sodium-glucose–linked transporter-1 (SGLT-1) and glucose transporter-2 (GLUT-2) were assessed before (T0), 1 hour (T1), 1 month (T2), 3 months (T3), and 6 months (T4) after embolization. Results. In group A, a segmental duodenal stenosis occurred in all cases, which required balloon dilatation. There was a significant drop in the baseline glycemia in group A at T1 and T4 versus sham. Ghrelin was reduced in group A versus baseline and versus group B at T2 and T3 and versus sham at T1 and T3. Insulin was significantly lower in group A versus B at T1 and at T4 but not versus sham. SGLT-1 expression increased in B and sham at T4, while it remained stable in group A. GLUT-2 expression increased in sham at T4 but not in A or B. Conclusions. GDA embolization induced a decrease in ghrelin production and influenced expression of glucose carriers in the foregut mucosa.


2005 ◽  
Vol 288 (2) ◽  
pp. E447-E453 ◽  
Author(s):  
April D. Strader ◽  
Torsten P. Vahl ◽  
Ronald J. Jandacek ◽  
Stephen C. Woods ◽  
David A. D’Alessio ◽  
...  

Bariatric surgeries, such as gastric bypass, result in dramatic and sustained weight loss that is usually attributed to a combination of gastric volume restriction and intestinal malabsorption. However, studies parceling out the contribution of enhanced intestinal stimulation in the absence of these two mechanisms have received little attention. Previous studies have demonstrated that patients who received intestinal bypass or Roux-en-Y surgery have increased release of gastrointestinal hormones. One possible mechanism for this increase is the rapid transit of nutrients into the intestine after eating. To determine whether there is increased secretion of anorectic peptides produced in the distal small intestine when this portion of the gut is given greater exposure to nutrients, we preformed ileal transpositions (IT) in rats. In this procedure, an isolated segment of ileum is transposed to the jejunum, resulting in an intestinal tract of normal length but an alteration in the normal distribution of endocrine cells along the gut. Rats with IT lost more weight ( P < 0.05) and consumed less food ( P < 0.05) than control rats with intestinal transections and reanastomosis without transposition. Weight loss in the IT rats was not due to malabsorption of nutrients. However, transposition of distal gut to a proximal location caused increased synthesis and release of the anorectic ileal hormones glucagon-like peptide-1 (GLP-1) and peptide YY (PYY; P < 0.01). The association of weight loss with increased release of GLP-1 and PYY suggests that procedures that promote gastrointestinal endocrine function can reduce energy intake. These findings support the importance of evaluating the contribution of gastrointestinal hormones to the weight loss seen with bariatric surgery.


2007 ◽  
Vol 293 (2) ◽  
pp. R635-R641 ◽  
Author(s):  
Maria A. Zafra ◽  
Filomena Molina ◽  
Amadeo Puerto

Learned flavor preferences can be established after intragastric nutrient administration by two different behavioral procedures, concurrent and sequential. In a concurrent procedure, two flavored stimuli are offered separately but at the same time on a daily basis: one stimulus is paired with the simultaneous intragastric administration of partially digested food and the other with physiological saline. In sequential learning, the two stimuli are presented during alternate sessions. Neural mechanisms underlying these learning modalities have yet to be fully elucidated. The aim of this study was to examine the role of vagal afferent fibers in the visceral processing of rewarding nutrients during concurrent ( experiment 1) and sequential ( experiment 2) flavor preference learning in Wistar rats. For this purpose, capsaicin, a neurotoxin that destroys slightly myelinated or unmyelinated sensory axons, was applied to the subdiaphragmatic region of the esophagus to selectively damage most of the vagal afferent pathways that originate in the gastrointestinal system. Results showed that capsaicin [1 mg of capsaicin dissolved in 1 ml of vehicle (10% Tween 80 in oil)] blocked acquisition of concurrent but not sequential flavor preference learning. These results are interpreted in terms of a dual neurobiological system involved in processing the rewarding effects of intragastrically administered nutrients. The vagus nerve, specifically capsaicin-sensitive vagal afferent fibers, would only be essential in concurrent flavor preference learning, which requires rapid processing of visceral information.


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