The Influence of Restricted Feeding on Glucagon-Like Peptide-1 (GLP-1)-Containing Cells in the Chicken Small Intestine

2013 ◽  
Vol 43 (2) ◽  
pp. 153-158 ◽  
Author(s):  
M. M. Monir ◽  
K. Hiramatsu ◽  
A. Yamasaki ◽  
K. Nishimura ◽  
T. Watanabe
Keyword(s):  
Small Intestine ◽  
Restricted Feeding ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Oral intake of slowly digestible α-glucan, isomaltodextrin, stimulates glucagon-like peptide-1 secretion in the small intestine of rats

2019 ◽  
Vol 123 (6) ◽  
pp. 619-626
Author(s):  
Yoshihiko Komuro ◽  
Takashi Kondo ◽  
Shingo Hino ◽  
Tatsuya Morita ◽  
Naomichi Nishimura
Keyword(s):  
Small Intestine ◽  
Oral Delivery ◽  
Oral Intake ◽  
Membrane Vesicles ◽  
Rat Small Intestine ◽  
Maize Starch ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

AbstractTo investigate whether oral intake of highly branched α-glucan isomaltodextrin (IMD) could stimulate ileal glucagon-like peptide-1 (GLP-1) secretion, we examined (1) the digestibility of IMD, (2) the digestion and absorption rates of IMD, in rat small intestine and (3) portal GLP-1 concentration in rats given IMD. In Expt 1, ileorectostomised rats were given a 3 % IMD diet for 10 d. Separately, a 16-h in vitro digestion of IMD, using porcine pancreatic α-amylase and brush-border membrane vesicles from rat small intestine, was conducted. In Expt 2, upon 24-h fasting, rats were given any of glucose, IMD and high-amylose maize starch (HAMS) (1 g/kg of body weight). In Expt 3, caecectomised rats were given 0·2 % neomycin sulphate and a 5 % IMD diet for 10 d. The in vivo and in vitro digestibility of IMD was 70–80 %. The fraction of IMD digested in vitro for the first 120 min was 67 % of that in maize starch. The AUC for 0–120 min of plasma glucose concentration was significantly lower in HAMS group and tended to be lower in IMD group than in the glucose group. Finally, we also observed that, when compared with control rats, glucose of IMD significantly stimulated and improved the concentration of portal active GLP-1 in antibiotic-administered, caecectomised rats. We concluded that IMD was slowly digested and the resulting glucose stimulated GLP-1 secretion in rat small intestine. Oral delivery of slowly released IMD glucose to the small intestine probably exerts important, yet unknown, physiological effects on the recipient.

GLP-1 secretion is enhanced directly in the ileum but indirectly in the duodenum by a newly identified potent stimulator, zein hydrolysate, in rats

2009 ◽  
Vol 297 (4) ◽  
pp. G663-G671 ◽  
Author(s):  
Tohru Hira ◽  
Taisuke Mochida ◽  
Kyoko Miyashita ◽  
Hiroshi Hara
Keyword(s):  
Small Intestine ◽  
Sampling Method ◽  
Rat Intestine ◽  
Mesenteric Vein ◽  
L Cells ◽  
Corn Protein ◽  
Before And After ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Dose Dependent

Glucagon-like peptide-1 (GLP-1) is released from enteroendocrine cells (L cells) in response to food ingestion. The mechanism by which dietary peptides stimulate GLP-1 secretion in the gut is unknown. In the present study, we found that a hydrolysate prepared from zein, a major corn protein [zein hydrolysate (ZeinH)], strongly stimulates GLP-1 secretion in enteroendocrine GLUTag cells. Stimulatory mechanisms of GLP-1 secretion induced by ZeinH were investigated in the rat small intestine under anesthesia. Blood was collected through a portal catheter before and after ZeinH administration into different sites of the small intestine. The duodenal, jejunal, and ileal administration of ZeinH induced dose-dependent increases in portal GLP-1 concentration. GLP-1 secretion in response to the ileal administration of ZeinH was higher than that in the duodenal or jejunal administration. Capsaicin treatment on esophageal vagal trunks abolished the GLP-1 secretion induced by duodenal ZeinH but did not affect the secretion induced by jejunal or ileal ZeinH. These results suggest that ZeinH in the jejunum or ileum directly stimulates GLP-1 secretion but duodenal ZeinH indirectly stimulates GLP-1 secretion via the vagal afferent nerve. A direct blood sampling method from the duodenal vein and ileal mesenteric vein revealed that ZeinH administered into the ligated duodenal loop enhanced GLP-1 concentration in the ileal mesenteric vein but not in the duodenal vein. This confirmed that ZeinH in the duodenum induces GLP-1 secretion from L cells located in the ileum by an indirect mechanism. These results indicate that a potent GLP-1-releasing peptide, ZeinH, induces GLP-1 secretion by direct and indirect mechanisms in the rat intestine.

scholarly journals Ghrelin Does Not Directly Stimulate Secretion of Glucagon-like Peptide-1

2019 ◽  
Vol 105 (1) ◽  
pp. 266-275 ◽  
Author(s):  
Sara Lind Jepsen ◽  
Esben Thyssen Vestergaard ◽  
Pierre Larraufie ◽  
Fiona Mary Gribble ◽  
Frank Reimann ◽  
...  
Keyword(s):  
Small Intestine ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Receptor Expression ◽  
Gastrointestinal Hormone ◽  
Ghrelin Receptor ◽  
L Cells ◽  
Mouse Small Intestine ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Abstract Context The gastrointestinal hormone ghrelin stimulates growth hormone secretion and appetite, but recent studies indicate that ghrelin also stimulates the secretion of the appetite-inhibiting and insulinotropic hormone glucagon-like peptide-1 (GLP-1). Objective To investigate the putative effect of ghrelin on GLP-1 secretion in vivo and in vitro. Subjects and Methods A randomized placebo-controlled crossover study was performed in eight hypopituitary subjects. Ghrelin or saline was infused intravenously (1 pmol/min × kg) after collection of baseline sample (0 min), and blood was subsequently collected at time 30, 60, 90, and 120 minutes. Mouse small intestine was perfused (n = 6) and GLP-1 output from perfused mouse small intestine was investigated in response to vascular ghrelin administration in the presence and absence of a simultaneous luminal glucose stimulus. Ghrelin receptor expression was quantified in human (n = 11) and mouse L-cells (n = 3) by RNA sequencing and RT-qPCR, respectively. Results Ghrelin did not affect GLP-1 secretion in humans (area under the curve [AUC; 0–120 min]: ghrelin infusion = 1.37 ± 0.05 min × nmol vs. saline infusion = 1.40 ± 0.06 min × nmol [P = 0.63]), but induced peripheral insulin resistance. Likewise, ghrelin did not stimulate GLP-1 secretion from the perfused mouse small intestine model (mean outputs during baseline/ghrelin infusion = 19.3 ± 1.6/25.5 ± 2.0 fmol/min, n = 6, P = 0.16), whereas glucose-dependent insulinotropic polypeptide administration, used as a positive control, doubled GLP-1 secretion (P < 0.001). Intraluminal glucose increased GLP-1 secretion by 4-fold (P < 0.001), which was not potentiated by ghrelin. Finally, gene expression of the ghrelin receptor was undetectable in mouse L-cells and marginal in human L-cells. Conclusions Ghrelin does not interact directly with the L-cell and does not directly affect GLP-1 secretion.

scholarly journals A role for exogenous GLP-1 in the management of postprandial hypoglycaemia after Roux-en-Y gastric bypass?

2019 ◽  
Vol 181 (3) ◽  
pp. C5-C8
Author(s):  
Caroline C Øhrstrøm ◽  
Filip K Knop
Keyword(s):  
Gastric Bypass ◽  
Small Intestine ◽  
Plasma Glucose ◽  
Receptor Agonist ◽  
Postprandial Plasma Glucose ◽  
Meal Intake ◽  
Symptom Scores ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Glucose Stimulated Insulin Secretion

Roux-en-Y gastric bypass (RYGB) is one of the most common and successful bariatric surgeries. However, more than half of RYGB-operated individuals may suffer from post-bariatric hypoglycaemia (PBH) characterised by traditional hypoglycaemic symptoms occurring 1 to 4 hours after meal intake. The mechanisms underlying PBH most likely relate to accelerated delivery of nutrients to the small intestine resulting in unretarded nutrient absorption, large elevations in postprandial plasma glucose concentrations (constituting a potent insulin secretory stimulus), and grossly elevated postprandial plasma levels of the insulinotropic gut-derived hormone glucagon-like peptide 1 (GLP-1) potentiating glucose-stimulated insulin secretion. Based on previous findings that circulating GLP-1 concentrations increased by ~100% during insulin-induced hypoglycaemia before but not after RYGB, Almby et al. explored whether exogenous GLP-1 may protect against PBH. They performed hyperinsulinaemic hypoglycaemic clamps with concomitant infusion of the GLP-1 analogue exenatide and saline, respectively, in individuals who had undergone RYGB surgery. Infusion with exenatide during hypoglycaemia had no plasma glucose-raising effects, did not increase the counterregulatory glucagon response, and did not affect symptom scores. In the present commentary, potentially important implications derived from the study by Almby et al. published in the August issue of EJE, are discussed in the light of previous observations on GLP-1 receptor agonist treatment in PBH. While the findings by Almby et al. do not provide a solution for patients with PBH, they contribute to the knowledge base needed to address the growing problem of PBH.

scholarly journals Glucagon-like peptide-1 modulates neurally evoked mucosal chloride secretion in guinea pig small intestine in vitro

2012 ◽  
Vol 302 (3) ◽  
pp. G352-G358 ◽  
Author(s):  
Sara Baldassano ◽  
Guo-Du Wang ◽  
Flavia Mulè ◽  
Jackie D. Wood
Keyword(s):  
Small Intestine ◽  
Guinea Pig ◽  
Receptor Antagonist ◽  
Vasoactive Intestinal Peptide ◽  
Short Circuit ◽  
Chloride Secretion ◽  
Dependent Manner ◽  
Evoked Responses ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Glucagon-like peptide-1 (GLP-1) acts at the G protein-coupled receptor, GLP-1R, to stimulate secretion of insulin and to inhibit secretion of glucagon and gastric acid. Involvement in mucosal secretory physiology has received negligible attention. We aimed to study involvement of GLP-1 in mucosal chloride secretion in the small intestine. Ussing chamber methods, in concert with transmural electrical field stimulation (EFS), were used to study actions on neurogenic chloride secretion. ELISA was used to study GLP-1R effects on neural release of acetylcholine (ACh). Intramural localization of GLP-1R was assessed with immunohistochemistry. Application of GLP-1 to serosal or mucosal sides of flat-sheet preparations in Ussing chambers did not change baseline short-circuit current ( Isc), which served as a marker for chloride secretion. Transmural EFS evoked neurally mediated biphasic increases in Iscthat had an initial spike-like rising phase followed by a sustained plateau-like phase. Blockade of the EFS-evoked responses by tetrodotoxin indicated that the responses were neurally mediated. Application of GLP-1 reduced the EFS-evoked biphasic responses in a concentration-dependent manner. The GLP-1 receptor antagonist exendin-(9–39) suppressed this action of GLP-1. The GLP-1 inhibitory action on EFS-evoked responses persisted in the presence of nicotinic or vasoactive intestinal peptide receptor antagonists but not in the presence of a muscarinic receptor antagonist. GLP-1 significantly reduced EFS-evoked ACh release. In the submucosal plexus, GLP-1R immunoreactivity (IR) was expressed by choline acetyltransferase-IR neurons, neuropeptide Y-IR neurons, somatostatin-IR neurons, and vasoactive intestinal peptide-IR neurons. Our results suggest that GLP-1R is expressed in guinea pig submucosal neurons and that its activation leads to a decrease in neurally evoked chloride secretion by suppressing release of ACh at neuroepithelial junctions in the enteric neural networks that control secretomotor functions.

A stereologic evaluation of glucagon-like peptide-1 (GLP-1) mucosal cells in the small intestine of the developing pig

2002 ◽  
Vol 205 (2) ◽  
pp. 153-157 ◽  
Author(s):  
C. Van Ginneken ◽  
K. Verlinden ◽  
F. Van Meir ◽  
S. Sys ◽  
A. Weyns
Keyword(s):  
Small Intestine ◽  
Mucosal Cells ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals Complete Sequences of Glucagon-like Peptide-1 from Human and Pig Small Intestine

1989 ◽  
Vol 264 (22) ◽  
pp. 12826-12829
Author(s):  
C Orskov ◽  
M Bersani ◽  
A H Johnsen ◽  
P Højrup ◽  
J J Holst
Keyword(s):  
Small Intestine ◽  
Complete Sequences ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

The release of GLP-1 and ghrelin, but not GIP and CCK, by glucose is dependent upon the length of small intestine exposed

2006 ◽  
Vol 291 (3) ◽  
pp. E647-E655 ◽  
Author(s):  
Tanya J. Little ◽  
Selena Doran ◽  
James H. Meyer ◽  
Andre J. P. M. Smout ◽  
Deirdre G. O'Donovan ◽  
...  
Keyword(s):  
Small Intestine ◽  
Plasma Concentrations ◽  
Pressure Waves ◽  
Dietary Carbohydrate ◽  
Short Segment ◽  
Entire Small Intestine ◽  
Proximal Small Intestine ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Insulinotropic Peptide

Previous observations suggest that glucagon-like peptide-1 (GLP-1) is released into the bloodstream only when dietary carbohydrate enters the duodenum at rates that exceed the absorptive capacity of the proximal small intestine to contact GLP-1 bearing mucosa in more distal bowel. The aims of this study were to determine the effects of modifying the length of small intestine exposed to glucose on plasma concentrations of GLP-1 and also glucose-dependent insulinotropic peptide (GIP), insulin, cholecystokinin (CCK) and ghrelin, and antropyloric pressures. Glucose was infused at 3.5 kcal/min into the duodenum of eight healthy males (age 18–59 yr) over 60 min on the first day into an isolated 60-cm segment of the proximal small intestine (“short-segment infusion”); on the second day, the same amount of glucose was infused with access to the entire small intestine (“long-segment infusion”). Plasma GLP-1 increased and ghrelin decreased ( P < 0.05 for both) during the long-, but not the short-, segment infusion. By contrast, increases in plasma CCK and GIP did not differ between days. The rises in blood glucose and plasma insulin were greater during the long- than during the short-segment infusion ( P < 0.05). During the long- but not the short-segment infusion, antral pressure waves (PWs) were suppressed ( P < 0.05). Isolated pyloric PWs and basal pyloric pressure were stimulated on both days. In conclusion, the release of GLP-1 and ghrelin, but not CCK and GIP, is dependent upon >60 cm of the intestine being exposed to glucose.

scholarly journals Expression of serotonin, somatostatin, and glucagon-like peptide 1 (GLP1) in the intestinal neuroendocrine cells of pigs fed with population rye type and hybrid rye type grains

2019 ◽  
Vol 75 (05) ◽  
pp. 6251-2019
Author(s):  
ANNA ZACHARKO-SIEMBIDA ◽  
MARCIN B. ARCISZEWSKI ◽  
JOSE LUIS VALVERDE PIEDRA ◽  
EWA TOMASZEWSKA ◽  
SYLWIA SZYMAŃCZYK ◽  
...  
Keyword(s):  
Small Intestine ◽  
Large Intestine ◽  
Neuroendocrine Cells ◽  
Hormone Balance ◽  
Gut Hormone ◽  
Hybrid Rye ◽  
A Cell ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
A Minor

Neuroendocrine cells (NEC) are a cell population in the gastrointestinal tract that plays a role in the regulation of the digestion process, satiety and nutrient homeostasis. NE cells express a variety of bioactive hormones that can undergo changes in response to different luminal stimuli, including multiple components, which are present in the diet. In recent years, a modern (hybrid) type of rye grain has been introduced to feed industry. The goal of the present study was to determine immunohistochemically whether the feeding of the pigs with population and hybrid rye grains may evoke adverse changes in the small and large intestines in terms of the expression of serotonin, glucagon-like peptide 1 (GLP1) and somatostatin. Feeding animals with population and hybrid rye grains resulted in a slight increase in serotonin-positive NE cells in the small intestine (but not in the large intestine). After feeding animals with population rye (but not with hybrid rye) grains, there was a decrease in the small intestine GLP1-immunoreactive NE cells was found. No changes in the expression of GLP1 were found in the large intestine of experimental animals. The numbers of somatostatin-IR NEC in the small and large intestines were not affected by feeding with either population or hybrid rye grains. In conclusion, we found that feeding pigs with hybrid and population rye grains started adaptive changes in NEC. However, those changes were not profound, which allows us to speculate that adverse effects of these rye grains have a minor (if any) impact on the gut hormone balance (and indirectly on the health status) of animals.

scholarly journals Cinnamaldehyde Induces Release of Cholecystokinin and Glucagon-Like Peptide 1 by Interacting with Transient Receptor Potential Ankyrin 1 in a Porcine Ex-Vivo Intestinal Segment Model

Animals ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 2262
Author(s):  
Elout Van Liefferinge ◽  
Maximiliano Müller ◽  
Noémie Van Noten ◽  
Jeroen Degroote ◽  
Shahram Niknafs ◽  
...  
Keyword(s):  
Small Intestine ◽  
Transient Receptor Potential ◽  
Ex Vivo ◽  
Receptor Potential ◽  
Intestinal Segment ◽  
Gastric Function ◽  
Segment Model ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Transient Receptor

Cinnamaldehyde and capsaicin have been reported to exert effects on the gastric function, mediated by the interaction with transient receptor potential ankyrin channel 1 (TRPA1) and transient receptor potential vanilloid channel 1 (TRPV1), respectively. This study examined whether these compounds could trigger the release of cholecystokinin (CCK) and/or glucagon-like peptide 1 (GLP-1) in the pig’s gut in a porcine ex-vivo intestinal segment model. Furthermore, it was verified whether this response was mediated by TRPA1 or TRPV1 by using the channel’s antagonist. These gut peptides play a key role in the “intestinal brake", a feedback mechanism that influences the function of proximal parts of the gut. Structural analogues of cinnamaldehyde were screened as well, to explore structure-dependent activation. Results showed a significant effect of capsaicin on GLP-1 release in the proximal small intestine, TRPV1 independent. TRPA1 showed to be strongly activated by cinnamaldehyde, both in proximal and distal small intestine, evidenced by the release of CCK and GLP-1, respectively. Out of all structural derivates, cinnamaldehyde showed the highest affinity for TRPA1, which elucidates the importance of the α,β-unsaturated aldehyde moiety. In conclusion, cinnamaldehyde as a TRPA1 agonist, is a promising candidate to modulate gastric function, by activating intestinal brake mechanisms.

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