Pancreatic secretion evoked by cholecystokinin and non‐cholecystokinin‐dependent duodenal stimuli via vagal afferent fibres in the rat.

Liu, Ying; Owyang, Chung

doi:10.1113/jphysiol.1996.sp021531

Cited by 50 publications

(38 citation statements)

References 31 publications

(49 reference statements)

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“…Although some evidence shows that vagotomy does not change or actually enhances the anorectic effect of exogenous 5-HT (22,27), other data suggest that peripheral 5-HT acts as a signal molecule in carbohydrate-induced inhibition of food intake, most likely through vagal afferent activation. For example, electrophysiological studies show that endogenously released 5-HT plays a major role in signal transmission evoked by luminal carbohydrates to stimulate vagal fibers (47,80), including nodose neurons (48,50,80). Vagal sensory fibers, which are important in the negative feedback cascade to inhibit food intake (78,79), are likely involved in 5-HT 3 -receptormediated suppression of intake observed in our study.…”

Section: Discussionmentioning

confidence: 83%

Serotonin-type 3 receptors mediate intestinal Polycose- and glucose-induced suppression of intake

Savastano¹,

Carelle²,

Covașă³

2005

American Journal of Physiology-Regulatory, Integrative and Comp

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Savastano, David M., Melissa Carelle, and Mihai Covasa. Serotonin-type 3 receptors mediate intestinal Polycose-and glucoseinduced suppression of intake. Am J Physiol Regul Integr Comp Physiol 288: R1499 -R1508, 2005. First published February 17, 2005 doi:10.1152/ajpregu.00745.2004.-Ondansetron, a selective serotonin-type 3 (5-HT3) receptor antagonist, was used to test the hypothesis that duodenal infusion of isosmotic solutions of Polycose or its hydrolytic product glucose suppressed intake through 5-HT3 receptors. Polycose suppressed sucrose intake across both concentrations infused (132 mM, 7.6 Ϯ 0.6 ml; 263 mM, 2.3 Ϯ 0.5 ml), compared with intake under control conditions (12.6 Ϯ 0.3 ml, P Ͻ0.001). Pretreatment with 1.0 mg/kg ondansetron attenuated reduction of sucrose intake induced only by the highest concentration of Polycose (4.6 Ϯ 0.8 ml, P ϭ 0.004). Dose-response testing revealed that suppression of food intake by 263 mM Polycose was equally attenuated by ondansetron administered at 1.0, 2.0, and 5.0 mg/kg but not when given at 0.125, 0.25, and 0.5 mg/kg. Acarbose, an ␣-glucosidase inhibitor, attenuated Polycose-induced suppression of food intake, and pretreatment with 1.0 mg/kg ondansetron had no further effect. Suppression of intake after 990 mM glucose but not mannitol infusion was attenuated by pretreatment with 1.0 mg/kg ondansetron. The competitive SGLT1 inhibitor, phloridzin, had no effect on 60-min 990 mM glucose-induced suppression of intake or the ability of ondansetron to attenuate this suppression of intake. Conversely, glucoseinduced suppression of intake was attenuated by phloridzin at earlier time points and further attenuated when rats were pretreated with 1.0 mg/kg ondansetron. Ondansetron administration alone had no effect on intake at any dose tested. We conclude that 5-HT 3 receptors participate in the inhibition of food intake by intraduodenal infusion of carbohydrate solutions through a posthydrolytic, preabsorptive mechanism. nutrient absorption; food intake; satiation THE PRESENCE OF NUTRIENTS in the intestine elicits signals essential to feedback control of ingestion. Considerable advances have been made in understanding the mechanisms by which nutrients in the intestine suppress intake in a number of species (30, 33), including rats (42, 51, 53) and humans (74). For example, it is well documented that intestinal carbohydrates reduce food intake in a dose-responsive manner (53, 76) by preabsorptive (63, 78) as well as postabsorptive (71) factors, largely through vagal afferent pathways (78, 79). However, the complete mechanism(s) by which intestinal oligosaccharides or monosaccharides is perceived to elicit negative feedback control of intake is not known. Administration of the ␣-glucosidase inhibitor, acarbose, attenuates reduction of food intake and c-Fos-immunoreactivity by maltotriose (62, 63). Moreover, inhibition of sodium-dependent glucose transporter 1 (SGLT 1 ) by intestinal phloridzin infusion fails to attenuate suppression of food intake and vagal afferent activation...

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Section: Discussionmentioning

confidence: 83%

Serotonin-type 3 receptors mediate intestinal Polycose- and glucose-induced suppression of intake

Savastano¹,

Carelle²,

Covașă³

2005

American Journal of Physiology-Regulatory, Integrative and Comp

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“…There are three enteric sites of response to 5-HT: 1) the intrinsic primary afferent neuron (IPAN) responsible for the peristaltic reflex and secretion (3,13,25,28,44); 2) extrinsic primary sensory nerves responsible for gut-to-central nervous system (6) or gut-to-pancreas (29,30,31) communications; and 3) myenteric neurons that express 5-HT 3 receptors (20,22,44,57). The first two sites (IPAN and extrinsic sensory nerve) are obviously located on the afferent limb of the response, but the myenteric neurons that participate in serotonergic neurotransmissions are located on the efferent limb of the response (32).…”

Section: Discussionmentioning

confidence: 99%

Slowing intestinal transit by PYY depends on serotonergic and opioid pathways

Lin

Neevel

Chen

2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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. Slowing intestinal transit by PYY depends on serotonergic and opioid pathways. Am J Physiol Gastrointest Liver Physiol 286: G558-G563, 2004; 10.1152/ ajpgi.00278.2003.-Slowing of intestinal transit by fat is abolished by immunoneutralization of peptide YY (PYY), demonstrating a key role for this gut peptide. How PYY slows intestinal transit is not known. We tested the hypothesis that the slowing of intestinal transit by PYY may depend on an ondansetron-sensitive serotonergic pathway and a naloxone-sensitive opioid pathway. In a fistulated dog model, occluding Foley catheters were used to compartmentalize the small intestine into proximal (between fistulas) and distal (beyond midgut fistula) half of gut. Buffer (pH 7.0) was perfused into both proximal and distal gut, and PYY was delivered intravenously. Ondansetron or naloxone was mixed with buffer and delivered into either the proximal or distal half of gut. Intestinal transit was measured across the proximal half of the gut. The slowing of intestinal transit by PYY was abolished when either ondansetron or naloxone was delivered into the proximal, but not the distal gut, to localize the two pathways to the efferent limb of the slowing response. In addition, 5-HT slows intestinal transit with marker recovery decreased from 76.2 Ϯ 3.6% (control) to 33.5 Ϯ 2.4% (5-HT) (P Ͻ 0.0001) but was reversed by naloxone delivered into the proximal gut with marker recovery increased to 79.9 Ϯ 7.2% (P Ͻ 0.0005). We conclude that the slowing of intestinal transit by PYY depends on serotonergic neurotransmission via an opioid pathway. ileal brake; intestinal motility; 5-HT; enteric nervous system PEPTIDE YY (PYY), a distal gut peptide released in response to a fatty meal, slows intestinal transit when administered intravenously (47). In addition to this slowing effect on intestinal transit, PYY is considered an inhibitory peptide, because it suppresses gastrin-stimulated acid secretion (1, 42), pancreatic exocrine secretion (1, 40), CCK release (41), and gastric emptying (47). These inhibitory effects of exogenous PYY suggest that it may be responsible for the ileal brake (49), a response that suppresses the digestive activities of the upper gastrointestinal tract when nutrients such as fat reach the distal gut. Immunoneutralization studies (38) confirmed that PYY is a key mediator of the slowing of intestinal transit by the fat-induced ileal brake. It is not known, however, how PYY slows intestinal transit.Previously, we created a fistulated dog model that divided the small intestine into proximal and distal segments. We used it to show that placing fat in the distal half of small intestine slowed transit in the proximal half of small intestine. Because the luminal content of the proximal and distal intestinal segments were not in continuity, this observation indicated that the fat-induced ileal brake occurred via a reflex, whereby the distal segment exposed to fat served as the afferent limb of the reflex and the proximal segment in which intestinal transit was measured serv...

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“…Interestingly, however, as mentioned previously, application of DB to GI cells stimulates the release of CCK (8,18). While CCK is generally considered a satiety hormone that exerts its effects through both vagal and nonvagal (humoral) routes at various peripheral and central targets (3,27,34), it is also believed to convey stimulusspecific information in a paracrine fashion at local sensory afferent terminals (15,36). If CCK is involved as a critical chemosensory signaling component, then pretreatment with devazepide, a CCK-1R antagonist, should abolish the early response to intraduodenal DB, compared with pretreatment with its vehicle.…”

Section: Experiments 1: Rats Rapidly Suppress Ongoing Intake In Re-mentioning

confidence: 99%

Ongoing ingestive behavior is rapidly suppressed by a preabsorptive, intestinal “bitter taste” cue

Schier

Davidson

Powley

2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Schier LA, Davidson TL, Powley TL. Ongoing ingestive behavior is rapidly suppressed by a preabsorptive, intestinal "bitter taste" cue. Am J Physiol Regul Integr Comp Physiol 301: R1557-R1568, 2011. First published August 24, 2011 doi:10.1152/ajpregu.00344.2011.-The discovery that cells in the gastrointestinal (GI) tract express the same molecular receptors and intracellular signaling components known to be involved in taste has generated great interest in potential functions of such post-oral "taste" receptors in the control of food intake. To determine whether taste cues in the GI tract are detected and can directly influence behavior, the present study used a microbehavioral analysis of intake, in which rats drank from lickometers that were programmed to simultaneously deliver a brief yoked infusion of a taste stimulus to the intestines. Specifically, in daily 30-min sessions, thirsty rats with indwelling intraduodenal catheters were trained to drink hypotonic (0.12 M) sodium chloride (NaCl) and simultaneously self-infuse a 0.12 M NaCl solution. Once trained, in a subsequent series of intestinal taste probe trials, rats reduced licking during a 6-min infusion period, when a bitter stimulus denatonium benzoate (DB; 10 mM) was added to the NaCl vehicle for infusion, apparently conditioning a mild taste aversion. Presentation of the DB in isomolar lithium chloride (LiCl) for intestinal infusions accelerated the development of the response across trials and strengthened the temporal resolution of the early licking suppression in response to the arrival of the DB in the intestine. In an experiment to evaluate whether CCK is involved as a paracrine signal in transducing the intestinal taste of DB, the CCK-1R antagonist devazepide partially blocked the response to intestinal DB. In contrast to their ability to detect and avoid the bitter taste in the intestine, rats did not modify their licking to saccharin intraduodenal probe infusions. The intestinal taste aversion paradigm developed here provides a sensitive and effective protocol for evaluating which tastants-and concentrations of tastants-in the lumen of the gut can control ingestion. chemoreceptor; gastrointestinal; denatonium benzoate; food learning; cholecystokinin CHEMORECEPTORS ARE INDISPENSABLE to the control of food intake. As taste receptors on the tongue and in the oral cavity, they supply signals critical for accepting and rejecting foods for consumption, promoting intake of palatable foods, and preparing the digestive system for the arrival of nutrients. Complementary to this early oral sensory processing, chemoreceptors in the stomach and intestines transduce signals from the lumen to adjust motility, secrete digestive enzymes, and initiate satiation (cf., 24). Accordingly, the gastrointestinal (GI) tract has been conventionally considered to have a more or less continuous sensory surface for tracking meals to engage and revise apposite and coordinated responses particular to the properties of the food and the body's physiological state. Despite th...

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Pancreatic secretion evoked by cholecystokinin and non‐cholecystokinin‐dependent duodenal stimuli via vagal afferent fibres in the rat.

Cited by 50 publications

References 31 publications

Serotonin-type 3 receptors mediate intestinal Polycose- and glucose-induced suppression of intake

Serotonin-type 3 receptors mediate intestinal Polycose- and glucose-induced suppression of intake

Slowing intestinal transit by PYY depends on serotonergic and opioid pathways

Ongoing ingestive behavior is rapidly suppressed by a preabsorptive, intestinal “bitter taste” cue

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