The Experts below are selected from a list of 282 Experts worldwide ranked by ideXlab platform

Jin-xia Zhu - One of the best experts on this subject based on the ideXlab platform.

  • Colonic submucosal 5-HT(3) receptor-mediated somatostatin-dependent secretoinhibitory pathway is suppressed in water-immersion restraint stressed rats.
    European journal of pharmacology, 2011
    Co-Authors: Hua Guo, Xiao-hui Zhang, Xiao-yan Feng, Yue Zhang, Zhong-ping Duan, Jin-xia Zhu
    Abstract:

    We have demonstrated that the activation of 5-hydroxytryptamine (5-HT) receptor 3 in the submucosal plexus suppresses 5-HT-induced Colonic ion Secretion by increasing submucosal somatostatin release. A number of psychological and physical stresses have impacts on the intestinal mucosal functions, including Secretion and the epithelial barrier. Whether the 5-HT(3) receptor-mediated somatostatin-dependent secretoinhibitory pathway in the rat distal colon is involved in the stress process is still unknown. The present study aims to investigate the effect of the water-immersion restraint stress on this inhibitory pathway and its underlying mechanisms. Mucosa/submucosa preparations from the rat distal colon were mounted in the Ussing chambers for the measurement of short-circuit current (I(SC)). Real-time PCR and western blot were performed to study the expression of the 5-HT(3) receptor, 5-HT(4) receptor, and somatostatin receptor 2. Radioimmunoassay was used to measure somatostatin release. After 2h of water-immersion restraint stress, the membrane resistance (Rte) of rat mucosa/submucosa preparations was significantly decreased, but the baseline I(SC) and 5-HT-induced I(SC) responses were significantly increased. The protein expression of the submucosal 5-HT(3) receptors and mucosal somatostatin receptor 2 were down-regulated, and the 5-HT-induced somatostatin release from the mucosa/submucosa preparations was significantly reduced in the stress group. Taken together, these results suggest that the 5-HT(3) receptor-mediated somatostatin-dependent secretoinhibitory pathway is suppressed in the water-immersion restraint stressed rats, which may contribute to the acute stress-induced increase in Colonic Secretion.

  • Colonic submucosal 5-HT3 receptor-mediated somatostatin-dependent secretoinhibitory pathway is suppressed in water-immersion restraint stressed rats
    European Journal of Pharmacology, 2011
    Co-Authors: Hua Guo, Xiao-hui Zhang, Xiao-yan Feng, Yue Zhang, Zhong-ping Duan, Jin-xia Zhu
    Abstract:

    We have demonstrated that the activation of 5-hydroxytryptamine (5-HT) receptor 3 in the submucosal plexus suppresses 5-HT-induced Colonic ion Secretion by increasing submucosal somatostatin release. A number of psychological and physical stresses have impacts on the intestinal mucosal functions, including Secretion and the epithelial barrier. Whether the 5-HT(3) receptor-mediated somatostatin-dependent secretoinhibitory pathway in the rat distal colon is involved in the stress process is still unknown. The present study aims to investigate the effect of the water-immersion restraint stress on this inhibitory pathway and its underlying mechanisms. Mucosa/submucosa preparations from the rat distal colon were mounted in the Ussing chambers for the measurement of short-circuit current (I(SC)). Real-time PCR and western blot were performed to study the expression of the 5-HT(3) receptor, 5-HT(4) receptor, and somatostatin receptor 2. Radioimmunoassay was used to measure somatostatin release. After 2h of water-immersion restraint stress, the membrane resistance (Rte) of rat mucosa/submucosa preparations was significantly decreased, but the baseline I(SC) and 5-HT-induced I(SC) responses were significantly increased. The protein expression of the submucosal 5-HT(3) receptors and mucosal somatostatin receptor 2 were down-regulated, and the 5-HT-induced somatostatin release from the mucosa/submucosa preparations was significantly reduced in the stress group. Taken together, these results suggest that the 5-HT(3) receptor-mediated somatostatin-dependent secretoinhibitory pathway is suppressed in the water-immersion restraint stressed rats, which may contribute to the acute stress-induced increase in Colonic Secretion.

Yasutada Akiba - One of the best experts on this subject based on the ideXlab platform.

  • gut microbiota produced tryptamine activates an epithelial g protein coupled receptor to increase Colonic Secretion
    Cell Host & Microbe, 2018
    Co-Authors: Yogesh Bhattarai, Yasutada Akiba, Brianna B Williams, Eric J Battaglioli, Weston R Whitaker, Lisa Till, Madhusudan Grover, David R Linden, Karunya K Kandimalla, Nicholas C Zachos
    Abstract:

    Tryptamine, a tryptophan-derived monoamine similar to 5-hydroxytryptamine (5-HT), is produced by gut bacteria and is abundant in human and rodent feces. However, the physiologic effect of tryptamine in the gastrointestinal (GI) tract remains unknown. Here, we show that the biological effects of tryptamine are mediated through the 5-HT4 receptor (5-HT4R), a G-protein-coupled receptor (GPCR) uniquely expressed in the Colonic epithelium. Tryptamine increases both ionic flux across the Colonic epithelium and fluid Secretion in colonoids from germ-free (GF) and humanized (ex-GF colonized with human stool) mice, consistent with increased intestinal Secretion. The secretory effect of tryptamine is dependent on 5-HT4R activation and is blocked by 5-HT4R antagonist and absent in 5-HT4R-/- mice. GF mice colonized by Bacteroides thetaiotaomicron engineered to produce tryptamine exhibit accelerated GI transit. Our study demonstrates an aspect of host physiology under control of a bacterial metabolite that can be exploited as a therapeutic modality. VIDEO ABSTRACT.

  • reduction of epithelial Secretion in male rat distal Colonic mucosa by bile acid receptor tgr5 agonist int 777 role of submucosal neurons
    Neurogastroenterology and Motility, 2016
    Co-Authors: Henri Duboc, Ganna Tolstanova, Pu-qing Yuan, Izumi Kaji, Mandy Biraud, Yasutada Akiba, Jonathan D. Kaunitz, Mulugeta Million
    Abstract:

    Background Recent evidence from rat neuron-free mucosa study suggests that the membrane bile acid receptor TGR5 decreases Colonic Secretion under basal and stimulated conditions. As submucosal neurons are key players in secretory processes and highly express TGR5, we investigated their role in TGR5 agonist-induced inhibition of Secretion and the pathways recruited. Methods TGR5 expression and localization were assessed in rat proximal (pC) and distal (dC) colon by qPCR and immunohistochemistry with double labeling for cholinergic neurons in whole-mount preparations. The influence of a selective (INT-777) or weak (ursodeoxycholic acid, UDCA) TGR5 agonist on Colonic Secretion was assessed in Ussing chambers, in dC preparation removing seromuscular ± submucosal tissues, in the presence of different inhibitors of Secretion pathways. Key Results TGR5 mRNA is expressed in full thickness dC and pC and immunoreactivity is located in colonocytes and pChAT-positive neurons. Addition of INT-777, and less potently UDCA, decreased Colonic Secretion in seromuscular stripped dC by −58.17± 2.6%. INT-777 effect on basal Secretion was reduced in neuron-free and TTX-treated mucosal-submucosal preparations. Atropine, hexamethonium, indomethacin, and L-NAME all reduced significantly INT-777's inhibitory effect while the 5-HT4 antagonist, RS-39604, and lidocaine abolished it. INT-777 inhibited stimulated Colonic Secretion induced by nicotine, but not cisapride, carbachol or PGE2. Conclusions & Inferences TGR5 activation inhibits basal and stimulated distal Colonic Secretion in rats by acting directly on epithelial cells and also inhibiting submucosal neurons. This could represent a counter-regulatory mechanism, at the submucosal level, of the known prosecretory effect of bile acids in the colon.

  • Reduction of epithelial Secretion in male rat distal Colonic mucosa by bile acid receptor TGR5 agonist, INT‐777: role of submucosal neurons
    Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society, 2016
    Co-Authors: Henri Duboc, Ganna Tolstanova, Pu-qing Yuan, Izumi Kaji, Mandy Biraud, Yasutada Akiba, Jonathan D. Kaunitz, Mulugeta Million, Yvette Taché
    Abstract:

    Background Recent evidence from rat neuron-free mucosa study suggests that the membrane bile acid receptor TGR5 decreases Colonic Secretion under basal and stimulated conditions. As submucosal neurons are key players in secretory processes and highly express TGR5, we investigated their role in TGR5 agonist-induced inhibition of Secretion and the pathways recruited. Methods TGR5 expression and localization were assessed in rat proximal (pC) and distal (dC) colon by qPCR and immunohistochemistry with double labeling for cholinergic neurons in whole-mount preparations. The influence of a selective (INT-777) or weak (ursodeoxycholic acid, UDCA) TGR5 agonist on Colonic Secretion was assessed in Ussing chambers, in dC preparation removing seromuscular ± submucosal tissues, in the presence of different inhibitors of Secretion pathways. Key Results TGR5 mRNA is expressed in full thickness dC and pC and immunoreactivity is located in colonocytes and pChAT-positive neurons. Addition of INT-777, and less potently UDCA, decreased Colonic Secretion in seromuscular stripped dC by −58.17± 2.6%. INT-777 effect on basal Secretion was reduced in neuron-free and TTX-treated mucosal-submucosal preparations. Atropine, hexamethonium, indomethacin, and L-NAME all reduced significantly INT-777's inhibitory effect while the 5-HT4 antagonist, RS-39604, and lidocaine abolished it. INT-777 inhibited stimulated Colonic Secretion induced by nicotine, but not cisapride, carbachol or PGE2. Conclusions & Inferences TGR5 activation inhibits basal and stimulated distal Colonic Secretion in rats by acting directly on epithelial cells and also inhibiting submucosal neurons. This could represent a counter-regulatory mechanism, at the submucosal level, of the known prosecretory effect of bile acids in the colon.

  • FFA3 activation inhibits nicotine-induced Secretion and motility in rat proximal colon
    The FASEB Journal, 2016
    Co-Authors: Izumi Kaji, Yasutada Akiba, Takafumi Furuyama, Jonathan D. Kaunitz
    Abstract:

    Short-chain fatty acids (SCFA) are microbial fermentation products that are absorbed from the colon. Although luminal SCFA stimulate Colonic Secretion and motility, we have recently reported that a...

Jonathan D. Kaunitz - One of the best experts on this subject based on the ideXlab platform.

  • reduction of epithelial Secretion in male rat distal Colonic mucosa by bile acid receptor tgr5 agonist int 777 role of submucosal neurons
    Neurogastroenterology and Motility, 2016
    Co-Authors: Henri Duboc, Ganna Tolstanova, Pu-qing Yuan, Izumi Kaji, Mandy Biraud, Yasutada Akiba, Jonathan D. Kaunitz, Mulugeta Million
    Abstract:

    Background Recent evidence from rat neuron-free mucosa study suggests that the membrane bile acid receptor TGR5 decreases Colonic Secretion under basal and stimulated conditions. As submucosal neurons are key players in secretory processes and highly express TGR5, we investigated their role in TGR5 agonist-induced inhibition of Secretion and the pathways recruited. Methods TGR5 expression and localization were assessed in rat proximal (pC) and distal (dC) colon by qPCR and immunohistochemistry with double labeling for cholinergic neurons in whole-mount preparations. The influence of a selective (INT-777) or weak (ursodeoxycholic acid, UDCA) TGR5 agonist on Colonic Secretion was assessed in Ussing chambers, in dC preparation removing seromuscular ± submucosal tissues, in the presence of different inhibitors of Secretion pathways. Key Results TGR5 mRNA is expressed in full thickness dC and pC and immunoreactivity is located in colonocytes and pChAT-positive neurons. Addition of INT-777, and less potently UDCA, decreased Colonic Secretion in seromuscular stripped dC by −58.17± 2.6%. INT-777 effect on basal Secretion was reduced in neuron-free and TTX-treated mucosal-submucosal preparations. Atropine, hexamethonium, indomethacin, and L-NAME all reduced significantly INT-777's inhibitory effect while the 5-HT4 antagonist, RS-39604, and lidocaine abolished it. INT-777 inhibited stimulated Colonic Secretion induced by nicotine, but not cisapride, carbachol or PGE2. Conclusions & Inferences TGR5 activation inhibits basal and stimulated distal Colonic Secretion in rats by acting directly on epithelial cells and also inhibiting submucosal neurons. This could represent a counter-regulatory mechanism, at the submucosal level, of the known prosecretory effect of bile acids in the colon.

  • Reduction of epithelial Secretion in male rat distal Colonic mucosa by bile acid receptor TGR5 agonist, INT‐777: role of submucosal neurons
    Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society, 2016
    Co-Authors: Henri Duboc, Ganna Tolstanova, Pu-qing Yuan, Izumi Kaji, Mandy Biraud, Yasutada Akiba, Jonathan D. Kaunitz, Mulugeta Million, Yvette Taché
    Abstract:

    Background Recent evidence from rat neuron-free mucosa study suggests that the membrane bile acid receptor TGR5 decreases Colonic Secretion under basal and stimulated conditions. As submucosal neurons are key players in secretory processes and highly express TGR5, we investigated their role in TGR5 agonist-induced inhibition of Secretion and the pathways recruited. Methods TGR5 expression and localization were assessed in rat proximal (pC) and distal (dC) colon by qPCR and immunohistochemistry with double labeling for cholinergic neurons in whole-mount preparations. The influence of a selective (INT-777) or weak (ursodeoxycholic acid, UDCA) TGR5 agonist on Colonic Secretion was assessed in Ussing chambers, in dC preparation removing seromuscular ± submucosal tissues, in the presence of different inhibitors of Secretion pathways. Key Results TGR5 mRNA is expressed in full thickness dC and pC and immunoreactivity is located in colonocytes and pChAT-positive neurons. Addition of INT-777, and less potently UDCA, decreased Colonic Secretion in seromuscular stripped dC by −58.17± 2.6%. INT-777 effect on basal Secretion was reduced in neuron-free and TTX-treated mucosal-submucosal preparations. Atropine, hexamethonium, indomethacin, and L-NAME all reduced significantly INT-777's inhibitory effect while the 5-HT4 antagonist, RS-39604, and lidocaine abolished it. INT-777 inhibited stimulated Colonic Secretion induced by nicotine, but not cisapride, carbachol or PGE2. Conclusions & Inferences TGR5 activation inhibits basal and stimulated distal Colonic Secretion in rats by acting directly on epithelial cells and also inhibiting submucosal neurons. This could represent a counter-regulatory mechanism, at the submucosal level, of the known prosecretory effect of bile acids in the colon.

  • FFA3 activation inhibits nicotine-induced Secretion and motility in rat proximal colon
    The FASEB Journal, 2016
    Co-Authors: Izumi Kaji, Yasutada Akiba, Takafumi Furuyama, Jonathan D. Kaunitz
    Abstract:

    Short-chain fatty acids (SCFA) are microbial fermentation products that are absorbed from the colon. Although luminal SCFA stimulate Colonic Secretion and motility, we have recently reported that a...

Henri Duboc - One of the best experts on this subject based on the ideXlab platform.

  • reduction of epithelial Secretion in male rat distal Colonic mucosa by bile acid receptor tgr5 agonist int 777 role of submucosal neurons
    Neurogastroenterology and Motility, 2016
    Co-Authors: Henri Duboc, Ganna Tolstanova, Pu-qing Yuan, Izumi Kaji, Mandy Biraud, Yasutada Akiba, Jonathan D. Kaunitz, Mulugeta Million
    Abstract:

    Background Recent evidence from rat neuron-free mucosa study suggests that the membrane bile acid receptor TGR5 decreases Colonic Secretion under basal and stimulated conditions. As submucosal neurons are key players in secretory processes and highly express TGR5, we investigated their role in TGR5 agonist-induced inhibition of Secretion and the pathways recruited. Methods TGR5 expression and localization were assessed in rat proximal (pC) and distal (dC) colon by qPCR and immunohistochemistry with double labeling for cholinergic neurons in whole-mount preparations. The influence of a selective (INT-777) or weak (ursodeoxycholic acid, UDCA) TGR5 agonist on Colonic Secretion was assessed in Ussing chambers, in dC preparation removing seromuscular ± submucosal tissues, in the presence of different inhibitors of Secretion pathways. Key Results TGR5 mRNA is expressed in full thickness dC and pC and immunoreactivity is located in colonocytes and pChAT-positive neurons. Addition of INT-777, and less potently UDCA, decreased Colonic Secretion in seromuscular stripped dC by −58.17± 2.6%. INT-777 effect on basal Secretion was reduced in neuron-free and TTX-treated mucosal-submucosal preparations. Atropine, hexamethonium, indomethacin, and L-NAME all reduced significantly INT-777's inhibitory effect while the 5-HT4 antagonist, RS-39604, and lidocaine abolished it. INT-777 inhibited stimulated Colonic Secretion induced by nicotine, but not cisapride, carbachol or PGE2. Conclusions & Inferences TGR5 activation inhibits basal and stimulated distal Colonic Secretion in rats by acting directly on epithelial cells and also inhibiting submucosal neurons. This could represent a counter-regulatory mechanism, at the submucosal level, of the known prosecretory effect of bile acids in the colon.

  • Reduction of epithelial Secretion in male rat distal Colonic mucosa by bile acid receptor TGR5 agonist, INT‐777: role of submucosal neurons
    Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society, 2016
    Co-Authors: Henri Duboc, Ganna Tolstanova, Pu-qing Yuan, Izumi Kaji, Mandy Biraud, Yasutada Akiba, Jonathan D. Kaunitz, Mulugeta Million, Yvette Taché
    Abstract:

    Background Recent evidence from rat neuron-free mucosa study suggests that the membrane bile acid receptor TGR5 decreases Colonic Secretion under basal and stimulated conditions. As submucosal neurons are key players in secretory processes and highly express TGR5, we investigated their role in TGR5 agonist-induced inhibition of Secretion and the pathways recruited. Methods TGR5 expression and localization were assessed in rat proximal (pC) and distal (dC) colon by qPCR and immunohistochemistry with double labeling for cholinergic neurons in whole-mount preparations. The influence of a selective (INT-777) or weak (ursodeoxycholic acid, UDCA) TGR5 agonist on Colonic Secretion was assessed in Ussing chambers, in dC preparation removing seromuscular ± submucosal tissues, in the presence of different inhibitors of Secretion pathways. Key Results TGR5 mRNA is expressed in full thickness dC and pC and immunoreactivity is located in colonocytes and pChAT-positive neurons. Addition of INT-777, and less potently UDCA, decreased Colonic Secretion in seromuscular stripped dC by −58.17± 2.6%. INT-777 effect on basal Secretion was reduced in neuron-free and TTX-treated mucosal-submucosal preparations. Atropine, hexamethonium, indomethacin, and L-NAME all reduced significantly INT-777's inhibitory effect while the 5-HT4 antagonist, RS-39604, and lidocaine abolished it. INT-777 inhibited stimulated Colonic Secretion induced by nicotine, but not cisapride, carbachol or PGE2. Conclusions & Inferences TGR5 activation inhibits basal and stimulated distal Colonic Secretion in rats by acting directly on epithelial cells and also inhibiting submucosal neurons. This could represent a counter-regulatory mechanism, at the submucosal level, of the known prosecretory effect of bile acids in the colon.

Chih-yen Chen - One of the best experts on this subject based on the ideXlab platform.

  • α-melanocyte stimulating hormone modulates the central acyl ghrelin-induced stimulation of feeding, gastrointestinal motility, and Colonic Secretion
    Drug design development and therapy, 2017
    Co-Authors: Hsien-hao Huang, Shi-chuan Chang, Liang-yu Chen, Ming-luen Doong, Chih-yen Chen
    Abstract:

    BACKGROUND Acyl ghrelin-induced intake depends on hypothalamic neuropeptide Y and agouti-related protein (AgRP) neurotransmitters. Intracerebroventricular (ICV) injection of AgRP increases feeding through competitive antagonism at melanocortin receptors. ICV administration of α-melanocyte stimulating hormone (α-MSH), a natural antagonist of AgRP, may modulate the acyl ghrelin-induced orexigenic effect. OBJECTIVE This study aimed to investigate the modulating effect of α-MSH on the central acyl ghrelin-induced food intake, gastrointestinal motility, and Colonic Secretion in rats. METHODS AND PROCEDURES We examined the effects of α-MSH and acyl ghrelin on food intake, gastric emptying, small intestinal transit, Colonic motility, and Secretion in conscious rats with a chronic implant of ICV catheters. RESULTS ICV injection of O-n-octanoylated ghrelin (0.1 nmol/rat) significantly increased the cumulative food intake up to 8 h (P

  • α melanocyte stimulating hormone modulates the central acyl ghrelin induced stimulation of feeding gastrointestinal motility and Colonic Secretion
    Drug Design Development and Therapy, 2017
    Co-Authors: Hsien-hao Huang, Shi-chuan Chang, Liang-yu Chen, Ming-luen Doong, Chih-yen Chen
    Abstract:

    BACKGROUND Acyl ghrelin-induced intake depends on hypothalamic neuropeptide Y and agouti-related protein (AgRP) neurotransmitters. Intracerebroventricular (ICV) injection of AgRP increases feeding through competitive antagonism at melanocortin receptors. ICV administration of α-melanocyte stimulating hormone (α-MSH), a natural antagonist of AgRP, may modulate the acyl ghrelin-induced orexigenic effect. OBJECTIVE This study aimed to investigate the modulating effect of α-MSH on the central acyl ghrelin-induced food intake, gastrointestinal motility, and Colonic Secretion in rats. METHODS AND PROCEDURES We examined the effects of α-MSH and acyl ghrelin on food intake, gastric emptying, small intestinal transit, Colonic motility, and Secretion in conscious rats with a chronic implant of ICV catheters. RESULTS ICV injection of O-n-octanoylated ghrelin (0.1 nmol/rat) significantly increased the cumulative food intake up to 8 h (P<0.01), enhanced non-nutrient semi-liquid gastric emptying (P<0.001), increased the geometric center and running percentage of small intestinal transit (P<0.001), accelerated Colonic transit time (P<0.05), and increased fecal pellet output (P<0.01) and total fecal weight (P<0.01). Pretreatment with ICV injection of α-MSH (1.0 and 2.0 nmol/rat) attenuated the acyl ghrelin-induced hyperphagic effect, fecal pellet output, and total fecal weight, while higher dose of α-MSH (2.0 nmol/rat) attenuated the increase in the geometric center of small intestinal transit (P<0.01). However, neither dose of α-MSH altered acyl ghrelin-stimulated gastroprokinetic effect, increase in the running percentage of small intestinal transit, nor accelerated Colonic transit time. CONCLUSION α-MSH is involved in central acyl ghrelin-elicited feeding, small intestinal transit, fecal pellet output, and fecal weight. α-MSH does not affect central acyl ghrelin-induced acceleration of gastric emptying and Colonic transit time in rats.

  • Correlation between Colonic Secretion and Colonic motility in rats: Role of ghrelin.
    World journal of gastroenterology, 2016
    Co-Authors: Hsien-hao Huang, Ching-heng Ting, Yu-fong Syu, Shi-chuan Chang, Chih-yen Chen
    Abstract:

    AIM To explore the relationship between Colonic secretory function and Colonic motility. METHODS Using a rat model chronically implanted with intracerebroventricular (ICV) and cecal catheters, we validated the correlation between Colonic Secretion and Colonic motor functions, as well as the role of ICV injection volume. RESULTS Compared to saline controls (5 μL/rat), ICV acyl ghrelin at 1 nmol/5 μL enhanced the total fecal weight, accelerated the Colonic transit time, and increased the fecal pellet output during the first hour post-injection, while ICV des-acyl ghrelin at 1 nmol/5 μL only accelerated the Colonic transit time. These stimulatory effects on Colonic motility and/or Secretion from acyl ghrelin and des-acyl ghrelin disappeared when the ICV injection volume increased to 10 μL compared with saline controls (10 μL/rat). Additionally, the ICV injection of 10 μL of saline significantly shortened the Colonic transit time compared with the ICV injection of 5 μL of saline. The total fecal weight during the first hour post-injection correlated with the Colonic transit time and fecal pellet output after the ICV injection of acyl ghrelin (1 nmol/5 μL), whereas the total fecal weight during the first hour post-injection correlated with the fecal pellet output but not the Colonic transit time after the ICV injection of des-acyl ghrelin (1 nmol/5 μL). CONCLUSION Colonic Secretion does not always correlate with Colonic motility in response to different Colonic stimulations. Acyl ghrelin stimulates Colonic Secretion.

  • Peripheral injection of pancreatic polypeptide enhances Colonic transit without eliciting anxiety or altering Colonic Secretion in rats
    Neuropeptides, 2015
    Co-Authors: Ching-heng Ting, Ying-chieh Chen, Wen-jinn Liaw, Han-chieh Lin, Chih-yen Chen
    Abstract:

    Pancreatic polypeptide (PP) is a negative regulator of energy homeostasis that suppresses food intake and lowers body weight. Similar to other gastrointestinal-derived peptides, PP also modulates gastrointestinal motility and may be involved in the regulation of anxiety. Previous studies revealed that PP suppresses gastric emptying but increases Colonic motility in mice. In our present study, we assessed the effect of PP on anxiety as well as Colonic motility and secretory function. Intracerebroventricular and intravenous routes of PP were administered in conscious rats. Our results showed that intracerebroventricular administration of PP did not affect anxiety in the open field test. Intravenous injection of PP accelerated Colonic transit, but did not significantly change fecal amount and fecal fluid composition. On the other hand, intracerebroventricular injection of PP did not alter Colonic transit, fecal amount, or fluid composition. In conclusion, peripheral, but not central PP administration enhances Colonic motility without eliciting anxiety or altering Colonic Secretion.