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  • the bitter tastant Denatonium Benzoate has no influence on the number of transient lower esophageal sphincter relaxations in health
    Neurogastroenterology and Motility, 2021
    Co-Authors: Hannelore Geysen, Jan Tack, Annelies Geeraerts, Wout Verbeure, Tim Vanuytsel, Ans Pauwels
    Abstract:

    BACKGROUND Administration of a bitter compound can alter the intragastric pressure (IGP) after a meal. Additionally, a negative correlation between IGP and the number of transient lower esophageal sphincter relaxations (TLESRs) has been demonstrated. However, the effect of a bitter tastant on the number of TLESRs and subsequent reflux episodes has never been investigated and it is unclear whether bitter food items should be avoided in gastro-esophageal reflux disease. We hypothesize that bitter administration in healthy volunteers (HVs) will lead to an increase in the number of TLESRs. METHODS After an overnight fast, 20 female HVs (36 years [21-63]) underwent a high-resolution impedance manometry (HRiM) measurement. After placement of the HRiM probe, 0.1 ml/kg of a 10 mM Denatonium Benzoate solution (bitter) or an identical volume of water (placebo) was administered directly into the stomach. The number of TLESRs and reflux episodes was quantified 30 min before and 2 h after consumption of a high caloric meal. KEY RESULTS There was no significant difference in the number of TLESRs or reflux episodes between the bitter and placebo condition. Additionally, no differences were observed in the nature (gas or liquid) and extent of reflux events. Lower esophageal sphincter pressures dropped significantly in the first postprandial hour to start recovering slowly back to baseline values during the second postprandial hour (p < 0.0001), without any difference between both conditions. CONCLUSIONS & INTERFERENCES Administration of the bitter tastant Denatonium Benzoate has no influence on the number of TLESRs or reflux episodes.

  • intragastric infusion of Denatonium Benzoate attenuates interdigestive gastric motility and hunger scores in healthy female volunteers
    The American Journal of Clinical Nutrition, 2017
    Co-Authors: Eveline Deloose, Inge Depoortere, Alessandra Rotondo, Pieter Janssen, Maura Corsetti, Jessica R Biesiekierski, Imke Masuy, Lukas Van Oudenhove, Jan Tack
    Abstract:

    Background: Denatonium Benzoate (DB) has been shown to influence ongoing ingestive behavior and gut peptide secretion. Objective: We studied how the intragastric administration of DB affects interdigestive motility, motilin and ghrelin plasma concentrations, hunger and satiety ratings, and food intake in healthy volunteers. Design: Lingual bitter taste sensitivity was tested with the use of 6 concentrations of DB in 65 subjects. A placebo or 1 μmol DB/kg was given intragastrically to assess its effect on fasting gastrointestinal motility and hunger ratings, motilin and ghrelin plasma concentrations, satiety, and caloric intake. Results: Women (n = 39) were more sensitive toward a lingual bitter stimulus (P = 0.005) than men (n = 26). In women (n = 10), intragastric DB switched the origin of phase III contractions from the stomach to the duodenum (P = 0.001) and decreased hunger ratings (P = 0.04). These effects were not observed in men (n = 10). In women (n = 12), motilin (P = 0.04) plasma concentrations decreased after intragastric DB administration, whereas total and octanoylated ghrelin were not affected. The intragastric administration of DB decreased hunger (P = 0.008) and increased satiety ratings (P = 0.01) after a meal (500 kcal) in 13 women without affecting gastric emptying in 6 women. Caloric intake tended to decrease after DB administration compared with the placebo (mean ± SEM: 720 ± 58 compared with 796 ± 45 kcal; P = 0.08) in 20 women. Conclusions: Intragastric DB administration decreases both antral motility and hunger ratings during the fasting state, possibly because of a decrease in motilin release. Moreover, DB decreases hunger and increases satiety ratings after a meal and shows potential for decreasing caloric intake

  • RESEARCH ARTICLE The Gustatory Signaling Pathway and Bitter Taste Receptors Affect the Development of Obesity and Adipocyte Metabolism in Mice
    2016
    Co-Authors: Bert Avau, Jan Tack, Dries Bauters, Laurien Vancleef, Jorien Laermans, Jens Lesuisse, Johan Buyse, Roger H. Lijnen, Ra Steensels, Inge Depoortere
    Abstract:

    Intestinal chemosensory signaling pathways involving the gustatory G-protein, gustducin, and bitter taste receptors (TAS2R) have been implicated in gut hormone release. Alterations in gut hormone profiles may contribute to the success of bariatric surgery. This study investi-gated the involvement of the gustatory signaling pathway in the development of diet-induced obesity and the therapeutic potential of targeting TAS2Rs to induce body weight loss. α-gust-ducin-deficient (α-gust-/-) mice became less obese than wild type (WT) mice when fed a high-fat diet (HFD). White adipose tissue (WAT) mass was lower in α-gust-/- mice due to increased heat production as a result of increases in brown adipose tissue (BAT) thermogenic activity, involving increased protein expression of uncoupling protein 1. Intra-gastric treatment of obeseWT and α-gust-/- mice with the bitter agonists Denatonium Benzoate (DB) or quinine (Q) during 4 weeks resulted in an α-gustducin-dependent decrease in body weight gain asso-ciated with a decrease in food intake (DB), but not involving major changes in gut peptide release. BothWAT and 3T3-F442A pre-adipocytes express TAS2Rs. Treatment of pre-adipo-cytes with DB or Q decreased differentiation into mature adipocytes. In conclusion, interfering with the gustatory signaling pathway protects against the development of HFD-induced obe-sity presumably through promoting BAT activity. Intra-gastric bitter treatment inhibits weight gain, possibly by directly affecting adipocyte metabolism

  • targeting extra oral bitter taste receptors modulates gastrointestinal motility with effects on satiation
    Scientific Reports, 2015
    Co-Authors: Bert Avau, Alessandra Rotondo, Theo Thijs, Christopher N Andrews, Pieter Janssen, Jan Tack, Inge Depoortere
    Abstract:

    Bitter taste receptors (TAS2Rs) are present in extra-oral tissues, including gut endocrine cells. This study explored the presence and mechanism of action of TAS2R agonists on gut smooth muscle in vitro and investigated functional effects of intra-gastric administration of TAS2R agonists on gastric motility and satiation. TAS2Rs and taste signalling elements were expressed in smooth muscle tissue along the mouse gut and in human gastric smooth muscle cells (hGSMC). Bitter tastants induced concentration and region-dependent contractility changes in mouse intestinal muscle strips. Contractions induced by Denatonium Benzoate (DB) in gastric fundus were mediated via increases in intracellular Ca2+ release and extracellular Ca2+-influx, partially masked by a hyperpolarizing K+-efflux. Intra-gastric administration of DB in mice induced a TAS2R-dependent delay in gastric emptying. In hGSMC, bitter compounds evoked Ca2+-rises and increased ERK-phosphorylation. Healthy volunteers showed an impaired fundic relaxation in response to nutrient infusion and a decreased nutrient volume tolerance and increased satiation during an oral nutrient challenge test after intra-gastric DB administration. These findings suggest a potential role for intestinal TAS2Rs as therapeutic targets to alter gastrointestinal motility and hence to interfere with hunger signalling.

  • The Gustatory Signaling Pathway and Bitter Taste Receptors Affect the Development of Obesity and Adipocyte Metabolism in Mice
    2015
    Co-Authors: Bert Avau, Jan Tack, Dries Bauters, Sandra Steensels, Laurien Vancleef, Jorien Laermans, Jens Lesuisse, Johan Buyse, Roger H. Lijnen, Inge Depoortere
    Abstract:

    Intestinal chemosensory signaling pathways involving the gustatory G-protein, gustducin, and bitter taste receptors (TAS2R) have been implicated in gut hormone release. Alterations in gut hormone profiles may contribute to the success of bariatric surgery. This study investigated the involvement of the gustatory signaling pathway in the development of diet-induced obesity and the therapeutic potential of targeting TAS2Rs to induce body weight loss. α-gustducin-deficient (α-gust-/-) mice became less obese than wild type (WT) mice when fed a high-fat diet (HFD). White adipose tissue (WAT) mass was lower in α-gust-/- mice due to increased heat production as a result of increases in brown adipose tissue (BAT) thermogenic activity, involving increased protein expression of uncoupling protein 1. Intra-gastric treatment of obese WT and α-gust-/- mice with the bitter agonists Denatonium Benzoate (DB) or quinine (Q) during 4 weeks resulted in an α-gustducin-dependent decrease in body weight gain associated with a decrease in food intake (DB), but not involving major changes in gut peptide release. Both WAT and 3T3-F442A pre-adipocytes express TAS2Rs. Treatment of pre-adipocytes with DB or Q decreased differentiation into mature adipocytes. In conclusion, interfering with the gustatory signaling pathway protects against the development of HFD-induced obesity presumably through promoting BAT activity. Intra-gastric bitter treatment inhibits weight gain, possibly by directly affecting adipocyte metabolism.

Andre H. Lawrence - One of the best experts on this subject based on the ideXlab platform.

Inge Depoortere - One of the best experts on this subject based on the ideXlab platform.

  • intragastric infusion of Denatonium Benzoate attenuates interdigestive gastric motility and hunger scores in healthy female volunteers
    The American Journal of Clinical Nutrition, 2017
    Co-Authors: Eveline Deloose, Inge Depoortere, Alessandra Rotondo, Pieter Janssen, Maura Corsetti, Jessica R Biesiekierski, Imke Masuy, Lukas Van Oudenhove, Jan Tack
    Abstract:

    Background: Denatonium Benzoate (DB) has been shown to influence ongoing ingestive behavior and gut peptide secretion. Objective: We studied how the intragastric administration of DB affects interdigestive motility, motilin and ghrelin plasma concentrations, hunger and satiety ratings, and food intake in healthy volunteers. Design: Lingual bitter taste sensitivity was tested with the use of 6 concentrations of DB in 65 subjects. A placebo or 1 μmol DB/kg was given intragastrically to assess its effect on fasting gastrointestinal motility and hunger ratings, motilin and ghrelin plasma concentrations, satiety, and caloric intake. Results: Women (n = 39) were more sensitive toward a lingual bitter stimulus (P = 0.005) than men (n = 26). In women (n = 10), intragastric DB switched the origin of phase III contractions from the stomach to the duodenum (P = 0.001) and decreased hunger ratings (P = 0.04). These effects were not observed in men (n = 10). In women (n = 12), motilin (P = 0.04) plasma concentrations decreased after intragastric DB administration, whereas total and octanoylated ghrelin were not affected. The intragastric administration of DB decreased hunger (P = 0.008) and increased satiety ratings (P = 0.01) after a meal (500 kcal) in 13 women without affecting gastric emptying in 6 women. Caloric intake tended to decrease after DB administration compared with the placebo (mean ± SEM: 720 ± 58 compared with 796 ± 45 kcal; P = 0.08) in 20 women. Conclusions: Intragastric DB administration decreases both antral motility and hunger ratings during the fasting state, possibly because of a decrease in motilin release. Moreover, DB decreases hunger and increases satiety ratings after a meal and shows potential for decreasing caloric intake

  • RESEARCH ARTICLE The Gustatory Signaling Pathway and Bitter Taste Receptors Affect the Development of Obesity and Adipocyte Metabolism in Mice
    2016
    Co-Authors: Bert Avau, Jan Tack, Dries Bauters, Laurien Vancleef, Jorien Laermans, Jens Lesuisse, Johan Buyse, Roger H. Lijnen, Ra Steensels, Inge Depoortere
    Abstract:

    Intestinal chemosensory signaling pathways involving the gustatory G-protein, gustducin, and bitter taste receptors (TAS2R) have been implicated in gut hormone release. Alterations in gut hormone profiles may contribute to the success of bariatric surgery. This study investi-gated the involvement of the gustatory signaling pathway in the development of diet-induced obesity and the therapeutic potential of targeting TAS2Rs to induce body weight loss. α-gust-ducin-deficient (α-gust-/-) mice became less obese than wild type (WT) mice when fed a high-fat diet (HFD). White adipose tissue (WAT) mass was lower in α-gust-/- mice due to increased heat production as a result of increases in brown adipose tissue (BAT) thermogenic activity, involving increased protein expression of uncoupling protein 1. Intra-gastric treatment of obeseWT and α-gust-/- mice with the bitter agonists Denatonium Benzoate (DB) or quinine (Q) during 4 weeks resulted in an α-gustducin-dependent decrease in body weight gain asso-ciated with a decrease in food intake (DB), but not involving major changes in gut peptide release. BothWAT and 3T3-F442A pre-adipocytes express TAS2Rs. Treatment of pre-adipo-cytes with DB or Q decreased differentiation into mature adipocytes. In conclusion, interfering with the gustatory signaling pathway protects against the development of HFD-induced obe-sity presumably through promoting BAT activity. Intra-gastric bitter treatment inhibits weight gain, possibly by directly affecting adipocyte metabolism

  • targeting extra oral bitter taste receptors modulates gastrointestinal motility with effects on satiation
    Scientific Reports, 2015
    Co-Authors: Bert Avau, Alessandra Rotondo, Theo Thijs, Christopher N Andrews, Pieter Janssen, Jan Tack, Inge Depoortere
    Abstract:

    Bitter taste receptors (TAS2Rs) are present in extra-oral tissues, including gut endocrine cells. This study explored the presence and mechanism of action of TAS2R agonists on gut smooth muscle in vitro and investigated functional effects of intra-gastric administration of TAS2R agonists on gastric motility and satiation. TAS2Rs and taste signalling elements were expressed in smooth muscle tissue along the mouse gut and in human gastric smooth muscle cells (hGSMC). Bitter tastants induced concentration and region-dependent contractility changes in mouse intestinal muscle strips. Contractions induced by Denatonium Benzoate (DB) in gastric fundus were mediated via increases in intracellular Ca2+ release and extracellular Ca2+-influx, partially masked by a hyperpolarizing K+-efflux. Intra-gastric administration of DB in mice induced a TAS2R-dependent delay in gastric emptying. In hGSMC, bitter compounds evoked Ca2+-rises and increased ERK-phosphorylation. Healthy volunteers showed an impaired fundic relaxation in response to nutrient infusion and a decreased nutrient volume tolerance and increased satiation during an oral nutrient challenge test after intra-gastric DB administration. These findings suggest a potential role for intestinal TAS2Rs as therapeutic targets to alter gastrointestinal motility and hence to interfere with hunger signalling.

  • The Gustatory Signaling Pathway and Bitter Taste Receptors Affect the Development of Obesity and Adipocyte Metabolism in Mice
    2015
    Co-Authors: Bert Avau, Jan Tack, Dries Bauters, Sandra Steensels, Laurien Vancleef, Jorien Laermans, Jens Lesuisse, Johan Buyse, Roger H. Lijnen, Inge Depoortere
    Abstract:

    Intestinal chemosensory signaling pathways involving the gustatory G-protein, gustducin, and bitter taste receptors (TAS2R) have been implicated in gut hormone release. Alterations in gut hormone profiles may contribute to the success of bariatric surgery. This study investigated the involvement of the gustatory signaling pathway in the development of diet-induced obesity and the therapeutic potential of targeting TAS2Rs to induce body weight loss. α-gustducin-deficient (α-gust-/-) mice became less obese than wild type (WT) mice when fed a high-fat diet (HFD). White adipose tissue (WAT) mass was lower in α-gust-/- mice due to increased heat production as a result of increases in brown adipose tissue (BAT) thermogenic activity, involving increased protein expression of uncoupling protein 1. Intra-gastric treatment of obese WT and α-gust-/- mice with the bitter agonists Denatonium Benzoate (DB) or quinine (Q) during 4 weeks resulted in an α-gustducin-dependent decrease in body weight gain associated with a decrease in food intake (DB), but not involving major changes in gut peptide release. Both WAT and 3T3-F442A pre-adipocytes express TAS2Rs. Treatment of pre-adipocytes with DB or Q decreased differentiation into mature adipocytes. In conclusion, interfering with the gustatory signaling pathway protects against the development of HFD-induced obesity presumably through promoting BAT activity. Intra-gastric bitter treatment inhibits weight gain, possibly by directly affecting adipocyte metabolism.

  • Su2072 The Bitter Taste Receptor Agonist Denatonium Benzoate Alters Intragastric Pressure Profiles During Nutrient Drink Test in Healthy Volunteers
    Gastroenterology, 2013
    Co-Authors: Christopher N Andrews, Inge Depoortere, Pieter Janssen, Eveline Deloose, Sofie Verschueren, Anne Maes, Jan Tack
    Abstract:

    Background: Bitter taste receptors are expressed in the stomach and the duodenum but their function is unclear. We assessed the effects of a potent bitter tastant on intragastric pressure (IGP, a measure of gastric accommodation) and satiation in response to a liquid meal. Methods: We conducted a single-blind crossover trial of 16 healthy volunteers (8 female; mean age 30±2 yrs; mean BMI 23.8±0.9) given 1 μmol/kg (0.1mL/kg) of a 10mM Denatonium Benzoate (DB) solution or placebo in random order on separate occasions at least 1 week apart. First, both a standard high-resolution manometry (HRM) catheter and a 4mm feeding catheter were positioned intra-gastrically via the nose with location confirmed by detection of the lower esophageal sphincter (LES) and/or fluoroscopy. After an adjustment period, DB or placebo was administered through the feeding catheter. After 30 min, nutrient drink (ND; 30% fat, 42% carbohydrate, 28% protein) was infused into the stomach at 60mL/ min until maximum satiation, at which point it was stopped. Satiation (scored on 0-5 scale) was assessed every minute. IGP was measured as average pressure over 5 channels in the proximal stomach at least 1cm below the LES, with 5-minute baseline measured 10 minutes before ND start. Outcomes were compared with paired t-test or Wilcoxon test as appropriate. All data are expressed as mean ± SEM unless otherwise stated. Results: Baseline IGP prior to ND infusion was similar between DB and placebo (Table). After DB treatment, the nutrientinduced drop in IGP from baseline (baseline-nadir) was inhibited (p=0.056) and delayed (p=0.007) compared to placebo. The total area under the IGP curve during nutrient infusion was significantly smaller after DB (p=0.021), consistent with attenuation of the gastric accommodation response (Figure). Satiation score at nadir IGP tended to be higher after DB vs placebo (p=0.087). The volume of ND ingested and the duration of the nutrient infusion were not statistically different between groups. No adverse effects were noted after either agent. Conclusion: The potent bitter tastant DB inhibits gastric accommodation to a meal, independently of taste receptor stimulation in the tongue. Themechanism and receptors involved in this action warrant further study.

Pieter Janssen - One of the best experts on this subject based on the ideXlab platform.

  • intragastric infusion of Denatonium Benzoate attenuates interdigestive gastric motility and hunger scores in healthy female volunteers
    The American Journal of Clinical Nutrition, 2017
    Co-Authors: Eveline Deloose, Inge Depoortere, Alessandra Rotondo, Pieter Janssen, Maura Corsetti, Jessica R Biesiekierski, Imke Masuy, Lukas Van Oudenhove, Jan Tack
    Abstract:

    Background: Denatonium Benzoate (DB) has been shown to influence ongoing ingestive behavior and gut peptide secretion. Objective: We studied how the intragastric administration of DB affects interdigestive motility, motilin and ghrelin plasma concentrations, hunger and satiety ratings, and food intake in healthy volunteers. Design: Lingual bitter taste sensitivity was tested with the use of 6 concentrations of DB in 65 subjects. A placebo or 1 μmol DB/kg was given intragastrically to assess its effect on fasting gastrointestinal motility and hunger ratings, motilin and ghrelin plasma concentrations, satiety, and caloric intake. Results: Women (n = 39) were more sensitive toward a lingual bitter stimulus (P = 0.005) than men (n = 26). In women (n = 10), intragastric DB switched the origin of phase III contractions from the stomach to the duodenum (P = 0.001) and decreased hunger ratings (P = 0.04). These effects were not observed in men (n = 10). In women (n = 12), motilin (P = 0.04) plasma concentrations decreased after intragastric DB administration, whereas total and octanoylated ghrelin were not affected. The intragastric administration of DB decreased hunger (P = 0.008) and increased satiety ratings (P = 0.01) after a meal (500 kcal) in 13 women without affecting gastric emptying in 6 women. Caloric intake tended to decrease after DB administration compared with the placebo (mean ± SEM: 720 ± 58 compared with 796 ± 45 kcal; P = 0.08) in 20 women. Conclusions: Intragastric DB administration decreases both antral motility and hunger ratings during the fasting state, possibly because of a decrease in motilin release. Moreover, DB decreases hunger and increases satiety ratings after a meal and shows potential for decreasing caloric intake

  • targeting extra oral bitter taste receptors modulates gastrointestinal motility with effects on satiation
    Scientific Reports, 2015
    Co-Authors: Bert Avau, Alessandra Rotondo, Theo Thijs, Christopher N Andrews, Pieter Janssen, Jan Tack, Inge Depoortere
    Abstract:

    Bitter taste receptors (TAS2Rs) are present in extra-oral tissues, including gut endocrine cells. This study explored the presence and mechanism of action of TAS2R agonists on gut smooth muscle in vitro and investigated functional effects of intra-gastric administration of TAS2R agonists on gastric motility and satiation. TAS2Rs and taste signalling elements were expressed in smooth muscle tissue along the mouse gut and in human gastric smooth muscle cells (hGSMC). Bitter tastants induced concentration and region-dependent contractility changes in mouse intestinal muscle strips. Contractions induced by Denatonium Benzoate (DB) in gastric fundus were mediated via increases in intracellular Ca2+ release and extracellular Ca2+-influx, partially masked by a hyperpolarizing K+-efflux. Intra-gastric administration of DB in mice induced a TAS2R-dependent delay in gastric emptying. In hGSMC, bitter compounds evoked Ca2+-rises and increased ERK-phosphorylation. Healthy volunteers showed an impaired fundic relaxation in response to nutrient infusion and a decreased nutrient volume tolerance and increased satiation during an oral nutrient challenge test after intra-gastric DB administration. These findings suggest a potential role for intestinal TAS2Rs as therapeutic targets to alter gastrointestinal motility and hence to interfere with hunger signalling.

  • Su2072 The Bitter Taste Receptor Agonist Denatonium Benzoate Alters Intragastric Pressure Profiles During Nutrient Drink Test in Healthy Volunteers
    Gastroenterology, 2013
    Co-Authors: Christopher N Andrews, Inge Depoortere, Pieter Janssen, Eveline Deloose, Sofie Verschueren, Anne Maes, Jan Tack
    Abstract:

    Background: Bitter taste receptors are expressed in the stomach and the duodenum but their function is unclear. We assessed the effects of a potent bitter tastant on intragastric pressure (IGP, a measure of gastric accommodation) and satiation in response to a liquid meal. Methods: We conducted a single-blind crossover trial of 16 healthy volunteers (8 female; mean age 30±2 yrs; mean BMI 23.8±0.9) given 1 μmol/kg (0.1mL/kg) of a 10mM Denatonium Benzoate (DB) solution or placebo in random order on separate occasions at least 1 week apart. First, both a standard high-resolution manometry (HRM) catheter and a 4mm feeding catheter were positioned intra-gastrically via the nose with location confirmed by detection of the lower esophageal sphincter (LES) and/or fluoroscopy. After an adjustment period, DB or placebo was administered through the feeding catheter. After 30 min, nutrient drink (ND; 30% fat, 42% carbohydrate, 28% protein) was infused into the stomach at 60mL/ min until maximum satiation, at which point it was stopped. Satiation (scored on 0-5 scale) was assessed every minute. IGP was measured as average pressure over 5 channels in the proximal stomach at least 1cm below the LES, with 5-minute baseline measured 10 minutes before ND start. Outcomes were compared with paired t-test or Wilcoxon test as appropriate. All data are expressed as mean ± SEM unless otherwise stated. Results: Baseline IGP prior to ND infusion was similar between DB and placebo (Table). After DB treatment, the nutrientinduced drop in IGP from baseline (baseline-nadir) was inhibited (p=0.056) and delayed (p=0.007) compared to placebo. The total area under the IGP curve during nutrient infusion was significantly smaller after DB (p=0.021), consistent with attenuation of the gastric accommodation response (Figure). Satiation score at nadir IGP tended to be higher after DB vs placebo (p=0.087). The volume of ND ingested and the duration of the nutrient infusion were not statistically different between groups. No adverse effects were noted after either agent. Conclusion: The potent bitter tastant DB inhibits gastric accommodation to a meal, independently of taste receptor stimulation in the tongue. Themechanism and receptors involved in this action warrant further study.

Michel Hupé - One of the best experts on this subject based on the ideXlab platform.