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Jan Tack - One of the best experts on this subject based on the ideXlab platform.

  • contribution of different triggers to the gastric Accommodation Reflex in humans
    American Journal of Physiology-gastrointestinal and Liver Physiology, 2009
    Co-Authors: Pieter Vanden Berghe, Pieter Janssen, Sebastien Kindt, Rita Vos, Jan Tack
    Abstract:

    Accommodation of the stomach consists of a vagally mediated relaxation of the proximal stomach, providing the meal with a reservoir. Our aim was to study whether, similar to other vagally mediated processes, the Accommodation Reflex is also determined by cephalic, oropharyngeal, gastric, and intestinal phases. Eleven healthy subjects underwent in randomized order five gastric barostat studies and two satiety drinking tests. In all studies, isobaric tone measurements (at minimal distending pressure + 2 mmHg) were performed 20 min before and 20 min after a nutrient stimulus. The stimuli included only visual and olfactory exposure to a meal (cephalic stimulation), taking liquid nutrient in the mouth without swallowing (sham feeding), ingestion of a 200-ml 300-kcal nutrient meal with blocked outflow to the pylorus (gastric retention), and meal infusion through a nasointestinal tube (duodenal instillation), or normal ingestion (control). During satiety testing, subjects ingested liquid nutrient at a fixed rate of 15 ml/min until maximum satiety, with an inflated or deflated intrapyloric balloon assembly. Progressively bigger gastric relaxatory responses were seen with cephalic stimulation (18 ± 19 ml), sham feeding (54 ± 21 ml), gastric retention (95 ± 47), duodenal instillation (144 ± 33), and control (232 ± 33 ml). The amount of nutrient ingested at maximum satiety was significantly lower with an inflated intrapyloric balloon (1,223 ± 103 vs. 1,392 ± 124 ml, P < 0.05). The Accommodation Reflex in humans lacks a cephalic phase, but it can be activated from the oropharynx, the stomach, and the duodenum. Blocking passage to the duodenum significantly decreases the amplitude of the Accommodation Reflex and induces early satiety.

  • influence of the selective serotonin re uptake inhibitor paroxetine on gastric sensorimotor function in humans
    Alimentary Pharmacology & Therapeutics, 2003
    Co-Authors: Jan Tack, Dorine Broekaert, B Coulie, Benjamin Fischler, Jozef Janssens
    Abstract:

    Summary Background : The role of 5-hydroxytryptamine in the control of gastric fundus tone in humans is still unknown. Selective 5-hydroxytryptamine re-uptake inhibitors act both centrally and peripherally to enhance the availability of physiologically released 5-hydroxytryptamine. Aim : To study the influence of a selective 5-hydroxytryptamine re-uptake inhibitor, paroxetine, on gastric fundus tone, on the perception to gastric distension and on gastric Accommodation to a meal. Methods : Sixteen healthy volunteers underwent a gastric barostat study on two occasions, after pre-treatment with placebo or paroxetine, 20 mg/day. Graded isobaric and isovolumetric distensions were performed and perception was scored by a questionnaire. Subsequently, the amplitude of the gastric Accommodation to a mixed liquid meal was also measured. Results : Pre-treatment with paroxetine did not alter the thresholds for perception and discomfort during isobaric (4.7 ± 2.3 vs. 4.0 ± 2.0 mmHg and 13.3 ± 3.1 vs. 12.7 ± 2.3 mmHg above the minimum intragastric distending pressure, N.S.) and isovolumetric (307 ± 90 vs. 417 ± 114 mL and 772 ± 74 vs. 750 ± 76 mL, N.S.) distensions. Paroxetine significantly enhanced the amplitude of the meal-induced fundus relaxation (136 ± 51 vs. 255 ± 43 mL, P < 0.05). Conclusions : Pre-treatment with paroxetine enhances gastric Accommodation to a meal. These data suggest that the release of 5-hydroxytryptamine, probably at the level of the enteric nervous system, is involved in the control of the Accommodation Reflex in humans, and that paroxetine may be beneficial to patients with impaired post-prandial fundus relaxation.

  • role of nitric oxide in the gastric Accommodation Reflex and in meal induced satiety in humans
    Gut, 2002
    Co-Authors: Jan Tack, Ingrid Demedts, A Meulemans, Jan A J Schuurkes, J Janssens
    Abstract:

    Aims: In humans, impaired gastric Accommodation is associated with early satiety and weight loss. In animals, Accommodation involves activation of gastric nitrergic neurones. Our aim was to study involvement of nitric oxide in gastric Accommodation and in meal induced satiety in humans. Methods: The effect of NG-monomethyl-l-arginine (l-NMMA) 4 mg/kg/h and 8 mg/kg/h on gastric compliance, on sensitivity to distension, and on gastric Accommodation was studied with a barostat in double blind, randomised, placebo controlled studies. The effect of l-NMMA 8 mg/kg/h on meal induced satiety was studied using a drinking test. Results: l-NMMA had no significant effect on fasting compliance and sensitivity. Ingestion of a meal induced a relaxation of 274 (15) ml which was significantly smaller after l-NMMA 4 mg/kg/h (132 (45) ml; p=0.03) or l-NMMA 8 mg/kg/h (82 (72) ml; p=0.03). l-NMMA 8 mg/kg/h significantly decreased the amount of food ingested at maximum satiety from 1058 (67) to 892 (73) kcal (p<0.01). Conclusion: In humans, fasting gastric tone and sensitivity to distension are not influenced by nitric oxide synthase inhibition, but the gastric Accommodation Reflex involves activation of nitrergic neurones. Inhibition of nitric oxide synthase impairs Accommodation and enhances meal induced satiety.

  • the physiology and the pathophysiology of the gastric Accommodation Reflex in man
    Verhandelingen - Koninklijke Academie voor Geneeskunde van België, 2000
    Co-Authors: Jan Tack
    Abstract:

    Summarizing the previous sections, we have demonstrated that the gastric Accommodation Reflex in man involves the release of serotonin and the activation of a nitrergic motor neuron. We observed that almost half of the patients with functional dyspepsia have an impaired Accommodation Reflex, and this is associated with early satiety and weight loss. Drug-induced inhibition of the Accommodation Reflex is able to induce early satiety in healthy subjects. Administration of the anti-migraine drug sumatriptan, an agonist at 5-HT1P receptors on gastric myenteric neurons, causes a relaxation of the proximal stomach in man through a nitrergic pathway. Pretreatment with sumatriptan is able to restore impaired Accommodation and to improve early satiety in patients with functional dyspepsia. We conclude from these data that fundus-relaxing drugs may have a therapeutic potential in functional dyspepsia, and we hypothesize that fundus-contracting drugs may have therapeutic potential in the treatment of obesity.

J Janssens - One of the best experts on this subject based on the ideXlab platform.

  • MOTILITY AND VISCERAL SENSATION Role of nitric oxide in the gastric Accommodation Reflex and in meal induced satiety in humans
    2016
    Co-Authors: J Tack, Ingrid Demedts, A Meulemans, Jan A J Schuurkes, J Janssens
    Abstract:

    Aims: In humans, impaired gastric Accommodation is associated with early satiety and weight loss. In animals, Accommodation involves activation of gastric nitrergic neurones. Our aim was to study involvement of nitric oxide in gastric Accommodation and in meal induced satiety in humans. Methods: The effect of NG-monomethyl-L-arginine (L-NMMA) 4 mg/kg/h and 8 mg/kg/h on gastric compliance, on sensitivity to distension, and on gastric Accommodation was studied with a barostat in double blind, randomised, placebo controlled studies. The effect of L-NMMA 8 mg/kg/h on meal induced satiety was studied using a drinking test. Results: L-NMMA had no significant effect on fasting compliance and sensitivity. Ingestion of a meal induced a relaxation of 274 (15) ml which was significantly smaller after L-NMMA 4 mg/kg/h (132 (45) ml; p=0.03) or L-NMMA 8 mg/kg/h (82 (72) ml; p=0.03). L-NMMA 8 mg/kg/h significantly decreased the amount of food ingested at maximum satiety from 1058 (67) to 892 (73) kcal (p<0.01). Conclusion: In humans, fasting gastric tone and sensitivity to distension are not influenced by nitric oxide synthase inhibition, but the gastric Accommodation Reflex involves activation of nitrergic neurones. Inhibition of nitric oxide synthase impairs Accommodation and enhances meal induced satiety

  • role of nitric oxide in the gastric Accommodation Reflex and in meal induced satiety in humans
    Gut, 2002
    Co-Authors: Jan Tack, Ingrid Demedts, A Meulemans, Jan A J Schuurkes, J Janssens
    Abstract:

    Aims: In humans, impaired gastric Accommodation is associated with early satiety and weight loss. In animals, Accommodation involves activation of gastric nitrergic neurones. Our aim was to study involvement of nitric oxide in gastric Accommodation and in meal induced satiety in humans. Methods: The effect of NG-monomethyl-l-arginine (l-NMMA) 4 mg/kg/h and 8 mg/kg/h on gastric compliance, on sensitivity to distension, and on gastric Accommodation was studied with a barostat in double blind, randomised, placebo controlled studies. The effect of l-NMMA 8 mg/kg/h on meal induced satiety was studied using a drinking test. Results: l-NMMA had no significant effect on fasting compliance and sensitivity. Ingestion of a meal induced a relaxation of 274 (15) ml which was significantly smaller after l-NMMA 4 mg/kg/h (132 (45) ml; p=0.03) or l-NMMA 8 mg/kg/h (82 (72) ml; p=0.03). l-NMMA 8 mg/kg/h significantly decreased the amount of food ingested at maximum satiety from 1058 (67) to 892 (73) kcal (p<0.01). Conclusion: In humans, fasting gastric tone and sensitivity to distension are not influenced by nitric oxide synthase inhibition, but the gastric Accommodation Reflex involves activation of nitrergic neurones. Inhibition of nitric oxide synthase impairs Accommodation and enhances meal induced satiety.

  • motility and visceral sensation role of nitric oxide in the gastric Accommodation Reflex and in meal induced satiety in humans
    2002
    Co-Authors: J Tack, Ingrid Demedts, A Meulemans, Jan A J Schuurkes, J Janssens
    Abstract:

    G -monomethyl-L-arginine (L-NMMA) 4 mg/kg/h and 8 mg/kg/h on gastric compliance, on sensitivity to distension, and on gastric Accommodation was studied with a barostat in double blind, randomised, placebo controlled studies. The effect of L-NMMA 8 mg/kg/h on meal induced satiety was studied using a drinking test. Results: L-NMMA had no significant effect on fasting compliance and sensitivity. Ingestion of a meal induced a relaxation of 274 (15) ml which was significantly smaller after L-NMMA 4 mg/kg/h (132 (45) ml; p=0.03) or L-NMMA 8 mg/kg/h (82 (72) ml; p=0.03). L-NMMA 8 mg/kg/h significantly decreased the amount of food ingested at maximum satiety from 1058 (67) to 892 (73) kcal (p<0.01). Conclusion: In humans, fasting gastric tone and sensitivity to distension are not influenced by nitric oxide synthase inhibition, but the gastric Accommodation Reflex involves activation of nitrergic neurones. Inhibition of nitric oxide synthase impairs Accommodation and enhances meal induced satiety.

Delgado Aros Sílvia - One of the best experts on this subject based on the ideXlab platform.

  • Effects of glucagon-like peptide-1-(7-36)amide (GLP-1) on gastric motor function in health and diabetes : potential mechanism of action /
    Bellaterra : Universitat Autònoma de Barcelona, 2004
    Co-Authors: Delgado Aros Sílvia
    Abstract:

    Consultable des del TDXTítol obtingut de la portada digitalitzadaEl Glucagon-like peptide-1 (GLP-1), un pèptid derivat del processament del proglucagó en les cè_lules L del jejúnum i del colon, inhibeix la secreció àcida gàstrica i el buidament gàstric, a més de reduir la capacitat d'ingesta. Els mecanismes d'acció del GLP-1 no estan clars. Hi ha dades que suggereixen que la inhibició de les funcions gàstriques per part del GLP-1 estan mitjançades pel nervi vagus. L'acomodació o relaxació gàstrica en resposta a la ingesta és un Reflex mitjançat pel vagus que dóna lloc a un increment del volum o capacitat gàstrica que impedeix l'increment de la pressió intragàstrica quan mengem, evitant així l'aparició de símptomes. La primera hipòtesi que vàrem plantejar va ser que el GLP-1 inhibeix el Reflex d'acomodació gàstrica i que això explicaria en part la reducció de la capacitat d'ingesta que s'observa en administrar el GLP-1. Per provar aquesta hipòtesi vàrem comparar els efectes d'una infusió endovenosa de GLP-1 i placebo, en voluntaris sans, sobre l'acomodació gàstrica postprandial (mesurada amb la tècnica SPECT), l'increment postprandial del polipèptid pancreàtic (marcador de funció vagal abdominal) i el volum d'un nutrient líquid (Ensure®) ingerit fins atansar la sacietat màxima. Els resultats del primer estudi van demostrar que el GLP-1 no inhibeix l'acomodació gàstrica postprandial; al contrari, va augmentar el volum gàstric en dejú i després del menjar. Això es va acompanyar per una marcada inhibició de la secreció de polipèptid pancreàtic, la qual està sota control vagal colinèrgic. Degut a que el to gàstric està mantingut per influència colinèrgica vagal, els resultats obtinguts són compatibles amb la hipòtesi de que el GLP-1 indueix relaxació gàstrica (augment de volum gàstric) per inhibició de les vies colinèrgiques vagals. Si aquesta hipòtesi fos certa, en cas de disfunció vagal o vagotomia, el GLP-1 no produiria relaxació gàstrica (augment de volum gàstric). Per provar aquesta segona hipòtesi, vàrem estudiar l'efecte de la mateixa infusió endovenosa de GLP-1, comparada amb placebo, en els volums gàstrics de subjectes amb neuropatia vagal diabètica. Vàrem comparar també els volums gàstrics dels malalts diabètics que rebien placebo amb els dels subjectes sans estudiats en el primer estudi presentat en aquesta tesi. Al contrari del que vàrem observar en subjectes sans, el GLP-1 no va augmentar el volum gàstric en malalts diabètics amb neuropatia vagal. Això suggereix que l'efecte del GLP-1 sobre el volum gàstric està mitjançat pel nervi vagus. Els malalts diabètics avaluats presentaven volums gàstrics, tan en dejú com després del menjar, similars als dels subjectes sans. El nervi vagus participa en el control del to o volum gàstric, però hi ha altres mecanismes que també hi participen. Es més, hi ha evidència de que el to gàstric pot ser controlat adequadament en absència de innervació vagal extrínseca. De manera que la troballa de la existència de volums gàstrics normals en malalts amb neuropatia vagal s'afegeix a la evidència de que, en cas d'alteració del Reflex principal vago-vagal, es produeix un mecanisme adaptatiu per preservar la resposta de relaxació gàstrica postprandial.Glucagon-like peptide-1 (GLP-1), a peptide derived from the processing of the proglucagon molecule in L cells of the jejunum and colon, inhibits gastric acid secretion and gastric emptying rate and it also decreases food consumption. It is still not clear how these effects of GLP-1 are mediated. There are data that suggest that GLP-1 inhibition of upper gastrointestinal functions is mediated through the vagus nerve. The Accommodation or relaxation of the stomach in response to meal ingestion is a vagally-mediated Reflex that increases gastric volume. This prevents the increase in intragastric pressure when food and fluid enter in the stomach, avoiding the development of symptoms. We hypothesized that GLP-1 inhibits the gastric Accommodation Reflex and that this effect could partly explain the reduced food consumption with GLP-1. To test this hypothesis, we compared, in healthy volunteers, the effects of intravenous infusion of GLP-1 and placebo, on postprandial gastric Accommodation (as measured by the SPECT technique), postprandial response of plasma human pancreatic polypeptide (a surrogate marker of vagal abdominal function) and the volume of a nutrient liquid meal (Ensure_) ingested at maximum satiation. The results of the first study showed that GLP-1 does not inhibit postprandial gastric Accommodation; on the contrary, it increased fasting and postprandial gastric volumes. This was accompanied by a marked inhibition of the pancreatic polypeptide release, which is under vagal cholinergic control. Since gastric tone is maintained by vagal cholinergic input, the results observed in our first study suggested that GLP-1 could induce gastric relaxation (increase gastric volume) by inhibition of vagal cholinergic pathways. If this hypothesis were true, one would predict that in the presence of vagal dysfunction or vagotomy, GLP-1 would not induce gastric relaxation (increase gastric volume). To test this second hypothesis we studied the effect of the same intravenous infusion of GLP-1, compared to placebo, on gastric volumes in a sample of subjects with diabetes affected with vagal neuropathy. We also compared gastric volumes in diabetic patients on placebo to those in the healthy subjects who participated in the first study presented in this thesis. In contrast to effects in health, GLP-1 did not increase gastric volume in diabetics with vagal neuropathy. This suggests that the effect of GLP-1 on gastric volume is dependent on vagal function. The diabetic patients evaluated had gastric volumes similar to those of healthy controls. The vagus nerve participates in the control of gastric volume or tone; however, there are other mechanisms involved. Furthermore, there is increasing evidence that gastric tone may be adequately controlled in the absence of extrinsic vagal innervation. Thus, we believe that the normal gastric volume response to a meal observed in the presence of vagal neuropathy adds to the growing evidence of the existence of an adaptive response preserving postprandial gastric relaxation when the main vago-vagal Reflex is impaired

  • Effects of Glucagon-like Peptide-1-(7-36)amide (GLP-1) on Gastric Motor Function in Health and Diabetes: Potential Mechanism of Action
    'Universitat Autonoma de Barcelona', 2003
    Co-Authors: Delgado Aros Sílvia
    Abstract:

    El Glucagon-like peptide-1 (GLP-1), un pèptid derivat del processament del proglucagó en les cè_lules L del jejúnum i del colon, inhibeix la secreció àcida gàstrica i el buidament gàstric, a més de reduir la capacitat d'ingesta. Els mecanismes d'acció del GLP-1 no estan clars. Hi ha dades que suggereixen que la inhibició de les funcions gàstriques per part del GLP-1 estan mitjançades pel nervi vagus.L'acomodació o relaxació gàstrica en resposta a la ingesta és un Reflex mitjançat pel vagus que dóna lloc a un increment del volum o capacitat gàstrica que impedeix l'increment de la pressió intragàstrica quan mengem, evitant així l'aparició de símptomes. La primera hipòtesi que vàrem plantejar va ser que el GLP-1 inhibeix el Reflex d'acomodació gàstrica i que això explicaria en part la reducció de la capacitat d'ingesta que s'observa en administrar el GLP-1. Per provar aquesta hipòtesi vàrem comparar els efectes d'una infusió endovenosa de GLP-1 i placebo, en voluntaris sans, sobre l'acomodació gàstrica postprandial (mesurada amb la tècnica SPECT), l'increment postprandial del polipèptid pancreàtic (marcador de funció vagal abdominal) i el volum d'un nutrient líquid (Ensure®) ingerit fins atansar la sacietat màxima. Els resultats del primer estudi van demostrar que el GLP-1 no inhibeix l'acomodació gàstrica postprandial; al contrari, va augmentar el volum gàstric en dejú i després del menjar. Això es va acompanyar per una marcada inhibició de la secreció de polipèptid pancreàtic, la qual està sota control vagal colinèrgic. Degut a que el to gàstric està mantingut per influència colinèrgica vagal, els resultats obtinguts són compatibles amb la hipòtesi de que el GLP-1 indueix relaxació gàstrica (augment de volum gàstric) per inhibició de les vies colinèrgiques vagals. Si aquesta hipòtesi fos certa, en cas de disfunció vagal o vagotomia, el GLP-1 no produiria relaxació gàstrica (augment de volum gàstric). Per provar aquesta segona hipòtesi, vàrem estudiar l'efecte de la mateixa infusió endovenosa de GLP-1, comparada amb placebo, en els volums gàstrics de subjectes amb neuropatia vagal diabètica. Vàrem comparar també els volums gàstrics dels malalts diabètics que rebien placebo amb els dels subjectes sans estudiats en el primer estudi presentat en aquesta tesi. Al contrari del que vàrem observar en subjectes sans, el GLP-1 no va augmentar el volum gàstric en malalts diabètics amb neuropatia vagal. Això suggereix que l'efecte del GLP-1 sobre el volum gàstric està mitjançat pel nervi vagus.Els malalts diabètics avaluats presentaven volums gàstrics, tan en dejú com després del menjar, similars als dels subjectes sans. El nervi vagus participa en el control del to o volum gàstric, però hi ha altres mecanismes que també hi participen. Es més, hi ha evidència de que el to gàstric pot ser controlat adequadament en absència de innervació vagal extrínseca. De manera que la troballa de la existència de volums gàstrics normals en malalts amb neuropatia vagal s'afegeix a la evidència de que, en cas d'alteració del Reflex principal vago-vagal, es produeix un mecanisme adaptatiu per preservar la resposta de relaxació gàstrica postprandial.Glucagon-like peptide-1 (GLP-1), a peptide derived from the processing of the proglucagon molecule in L cells of the jejunum and colon, inhibits gastric acid secretion and gastric emptying rate and it also decreases food consumption. It is still not clear how these effects of GLP-1 are mediated. There are data that suggest that GLP-1 inhibition of upper gastrointestinal functions is mediated through the vagus nerve.The Accommodation or relaxation of the stomach in response to meal ingestion is a vagally-mediated Reflex that increases gastric volume. This prevents the increase in intragastric pressure when food and fluid enter in the stomach, avoiding the development of symptoms. We hypothesized that GLP-1 inhibits the gastric Accommodation Reflex and that this effect could partly explain the reduced food consumption with GLP-1. To test this hypothesis, we compared, in healthy volunteers, the effects of intravenous infusion of GLP-1 and placebo, on postprandial gastric Accommodation (as measured by the SPECT technique), postprandial response of plasma human pancreatic polypeptide (a surrogate marker of vagal abdominal function) and the volume of a nutrient liquid meal (Ensure_) ingested at maximum satiation. The results of the first study showed that GLP-1 does not inhibit postprandial gastric Accommodation; on the contrary, it increased fasting and postprandial gastric volumes. This was accompanied by a marked inhibition of the pancreatic polypeptide release, which is under vagal cholinergic control. Since gastric tone is maintained by vagal cholinergic input, the results observed in our first study suggested that GLP-1 could induce gastric relaxation (increase gastric volume) by inhibition of vagal cholinergic pathways. If this hypothesis were true, one would predict that in the presence of vagal dysfunction or vagotomy, GLP-1 would not induce gastric relaxation (increase gastric volume). To test this second hypothesis we studied the effect of the same intravenous infusion of GLP-1, compared to placebo, on gastric volumes in a sample of subjects with diabetes affected with vagal neuropathy. We also compared gastric volumes in diabetic patients on placebo to those in the healthy subjects who participated in the first study presented in this thesis. In contrast to effects in health, GLP-1 did not increase gastric volume in diabetics with vagal neuropathy. This suggests that the effect of GLP-1 on gastric volume is dependent on vagal function. The diabetic patients evaluated had gastric volumes similar to those of healthy controls. The vagus nerve participates in the control of gastric volume or tone; however, there are other mechanisms involved. Furthermore, there is increasing evidence that gastric tone may be adequately controlled in the absence of extrinsic vagal innervation. Thus, we believe that the normal gastric volume response to a meal observed in the presence of vagal neuropathy adds to the growing evidence of the existence of an adaptive response preserving postprandial gastric relaxation when the main vago-vagal Reflex is impaired

Ingrid Demedts - One of the best experts on this subject based on the ideXlab platform.

  • MOTILITY AND VISCERAL SENSATION Role of nitric oxide in the gastric Accommodation Reflex and in meal induced satiety in humans
    2016
    Co-Authors: J Tack, Ingrid Demedts, A Meulemans, Jan A J Schuurkes, J Janssens
    Abstract:

    Aims: In humans, impaired gastric Accommodation is associated with early satiety and weight loss. In animals, Accommodation involves activation of gastric nitrergic neurones. Our aim was to study involvement of nitric oxide in gastric Accommodation and in meal induced satiety in humans. Methods: The effect of NG-monomethyl-L-arginine (L-NMMA) 4 mg/kg/h and 8 mg/kg/h on gastric compliance, on sensitivity to distension, and on gastric Accommodation was studied with a barostat in double blind, randomised, placebo controlled studies. The effect of L-NMMA 8 mg/kg/h on meal induced satiety was studied using a drinking test. Results: L-NMMA had no significant effect on fasting compliance and sensitivity. Ingestion of a meal induced a relaxation of 274 (15) ml which was significantly smaller after L-NMMA 4 mg/kg/h (132 (45) ml; p=0.03) or L-NMMA 8 mg/kg/h (82 (72) ml; p=0.03). L-NMMA 8 mg/kg/h significantly decreased the amount of food ingested at maximum satiety from 1058 (67) to 892 (73) kcal (p<0.01). Conclusion: In humans, fasting gastric tone and sensitivity to distension are not influenced by nitric oxide synthase inhibition, but the gastric Accommodation Reflex involves activation of nitrergic neurones. Inhibition of nitric oxide synthase impairs Accommodation and enhances meal induced satiety

  • role of nitric oxide in the gastric Accommodation Reflex and in meal induced satiety in humans
    Gut, 2002
    Co-Authors: Jan Tack, Ingrid Demedts, A Meulemans, Jan A J Schuurkes, J Janssens
    Abstract:

    Aims: In humans, impaired gastric Accommodation is associated with early satiety and weight loss. In animals, Accommodation involves activation of gastric nitrergic neurones. Our aim was to study involvement of nitric oxide in gastric Accommodation and in meal induced satiety in humans. Methods: The effect of NG-monomethyl-l-arginine (l-NMMA) 4 mg/kg/h and 8 mg/kg/h on gastric compliance, on sensitivity to distension, and on gastric Accommodation was studied with a barostat in double blind, randomised, placebo controlled studies. The effect of l-NMMA 8 mg/kg/h on meal induced satiety was studied using a drinking test. Results: l-NMMA had no significant effect on fasting compliance and sensitivity. Ingestion of a meal induced a relaxation of 274 (15) ml which was significantly smaller after l-NMMA 4 mg/kg/h (132 (45) ml; p=0.03) or l-NMMA 8 mg/kg/h (82 (72) ml; p=0.03). l-NMMA 8 mg/kg/h significantly decreased the amount of food ingested at maximum satiety from 1058 (67) to 892 (73) kcal (p<0.01). Conclusion: In humans, fasting gastric tone and sensitivity to distension are not influenced by nitric oxide synthase inhibition, but the gastric Accommodation Reflex involves activation of nitrergic neurones. Inhibition of nitric oxide synthase impairs Accommodation and enhances meal induced satiety.

  • motility and visceral sensation role of nitric oxide in the gastric Accommodation Reflex and in meal induced satiety in humans
    2002
    Co-Authors: J Tack, Ingrid Demedts, A Meulemans, Jan A J Schuurkes, J Janssens
    Abstract:

    G -monomethyl-L-arginine (L-NMMA) 4 mg/kg/h and 8 mg/kg/h on gastric compliance, on sensitivity to distension, and on gastric Accommodation was studied with a barostat in double blind, randomised, placebo controlled studies. The effect of L-NMMA 8 mg/kg/h on meal induced satiety was studied using a drinking test. Results: L-NMMA had no significant effect on fasting compliance and sensitivity. Ingestion of a meal induced a relaxation of 274 (15) ml which was significantly smaller after L-NMMA 4 mg/kg/h (132 (45) ml; p=0.03) or L-NMMA 8 mg/kg/h (82 (72) ml; p=0.03). L-NMMA 8 mg/kg/h significantly decreased the amount of food ingested at maximum satiety from 1058 (67) to 892 (73) kcal (p<0.01). Conclusion: In humans, fasting gastric tone and sensitivity to distension are not influenced by nitric oxide synthase inhibition, but the gastric Accommodation Reflex involves activation of nitrergic neurones. Inhibition of nitric oxide synthase impairs Accommodation and enhances meal induced satiety.

Jan A J Schuurkes - One of the best experts on this subject based on the ideXlab platform.

  • MOTILITY AND VISCERAL SENSATION Role of nitric oxide in the gastric Accommodation Reflex and in meal induced satiety in humans
    2016
    Co-Authors: J Tack, Ingrid Demedts, A Meulemans, Jan A J Schuurkes, J Janssens
    Abstract:

    Aims: In humans, impaired gastric Accommodation is associated with early satiety and weight loss. In animals, Accommodation involves activation of gastric nitrergic neurones. Our aim was to study involvement of nitric oxide in gastric Accommodation and in meal induced satiety in humans. Methods: The effect of NG-monomethyl-L-arginine (L-NMMA) 4 mg/kg/h and 8 mg/kg/h on gastric compliance, on sensitivity to distension, and on gastric Accommodation was studied with a barostat in double blind, randomised, placebo controlled studies. The effect of L-NMMA 8 mg/kg/h on meal induced satiety was studied using a drinking test. Results: L-NMMA had no significant effect on fasting compliance and sensitivity. Ingestion of a meal induced a relaxation of 274 (15) ml which was significantly smaller after L-NMMA 4 mg/kg/h (132 (45) ml; p=0.03) or L-NMMA 8 mg/kg/h (82 (72) ml; p=0.03). L-NMMA 8 mg/kg/h significantly decreased the amount of food ingested at maximum satiety from 1058 (67) to 892 (73) kcal (p<0.01). Conclusion: In humans, fasting gastric tone and sensitivity to distension are not influenced by nitric oxide synthase inhibition, but the gastric Accommodation Reflex involves activation of nitrergic neurones. Inhibition of nitric oxide synthase impairs Accommodation and enhances meal induced satiety

  • role of nitric oxide in the gastric Accommodation Reflex and in meal induced satiety in humans
    Gut, 2002
    Co-Authors: Jan Tack, Ingrid Demedts, A Meulemans, Jan A J Schuurkes, J Janssens
    Abstract:

    Aims: In humans, impaired gastric Accommodation is associated with early satiety and weight loss. In animals, Accommodation involves activation of gastric nitrergic neurones. Our aim was to study involvement of nitric oxide in gastric Accommodation and in meal induced satiety in humans. Methods: The effect of NG-monomethyl-l-arginine (l-NMMA) 4 mg/kg/h and 8 mg/kg/h on gastric compliance, on sensitivity to distension, and on gastric Accommodation was studied with a barostat in double blind, randomised, placebo controlled studies. The effect of l-NMMA 8 mg/kg/h on meal induced satiety was studied using a drinking test. Results: l-NMMA had no significant effect on fasting compliance and sensitivity. Ingestion of a meal induced a relaxation of 274 (15) ml which was significantly smaller after l-NMMA 4 mg/kg/h (132 (45) ml; p=0.03) or l-NMMA 8 mg/kg/h (82 (72) ml; p=0.03). l-NMMA 8 mg/kg/h significantly decreased the amount of food ingested at maximum satiety from 1058 (67) to 892 (73) kcal (p<0.01). Conclusion: In humans, fasting gastric tone and sensitivity to distension are not influenced by nitric oxide synthase inhibition, but the gastric Accommodation Reflex involves activation of nitrergic neurones. Inhibition of nitric oxide synthase impairs Accommodation and enhances meal induced satiety.

  • motility and visceral sensation role of nitric oxide in the gastric Accommodation Reflex and in meal induced satiety in humans
    2002
    Co-Authors: J Tack, Ingrid Demedts, A Meulemans, Jan A J Schuurkes, J Janssens
    Abstract:

    G -monomethyl-L-arginine (L-NMMA) 4 mg/kg/h and 8 mg/kg/h on gastric compliance, on sensitivity to distension, and on gastric Accommodation was studied with a barostat in double blind, randomised, placebo controlled studies. The effect of L-NMMA 8 mg/kg/h on meal induced satiety was studied using a drinking test. Results: L-NMMA had no significant effect on fasting compliance and sensitivity. Ingestion of a meal induced a relaxation of 274 (15) ml which was significantly smaller after L-NMMA 4 mg/kg/h (132 (45) ml; p=0.03) or L-NMMA 8 mg/kg/h (82 (72) ml; p=0.03). L-NMMA 8 mg/kg/h significantly decreased the amount of food ingested at maximum satiety from 1058 (67) to 892 (73) kcal (p<0.01). Conclusion: In humans, fasting gastric tone and sensitivity to distension are not influenced by nitric oxide synthase inhibition, but the gastric Accommodation Reflex involves activation of nitrergic neurones. Inhibition of nitric oxide synthase impairs Accommodation and enhances meal induced satiety.