The Experts below are selected from a list of 243 Experts worldwide ranked by ideXlab platform
Christopher K Rayner - One of the best experts on this subject based on the ideXlab platform.
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Role of intestinal Glucose Absorption in Glucose tolerance.
Current opinion in pharmacology, 2020Co-Authors: Christopher K Rayner, Karen L Jones, Cong Xie, Chinmay S. Marathe, Michael HorowitzAbstract:Intestinal Glucose Absorption is integral to postprandial Glucose homeostasis. Glucose Absorption is dependent on a number of factors, including the exposure of carbohydrate to the mucosa of the upper gastrointestinal tract (determined particularly by the rates of gastric emptying and small intestinal transit), the digestion of complex carbohydrate into monosaccharides, and Glucose sensing and transport by the intestinal mucosa. The Absorption of Glucose in the small intestine is not only a determinant of the appearance of exogenous Glucose in the peripheral circulation, but is also coupled to the release of gastrointestinal hormones that in turn influence postprandial Glucose metabolism through modulating gastrointestinal motor function, insulin and glucagon secretion, and subsequent energy intake. This review describes the physiology and pathophysiology of intestinal Glucose Absorption in health and type 2 diabetes, including its relevance to Glucose tolerance and the management of postprandial hyperglycaemia.
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metformin reduces the rate of small intestinal Glucose Absorption in type 2 diabetes
Diabetes Obesity and Metabolism, 2017Co-Authors: Michael Horowitz, Karen L Jones, Cong Xie, Christopher K RaynerAbstract:In rodents, metformin slows intestinal Glucose Absorption, potentially increasing exposure of the distal gut to Glucose to enhance postprandial glucagon-like peptide-1 (GLP-1) secretion. We evaluated the effects of metformin on serum 3-O-methylGlucose (3-OMG; a marker of Glucose Absorption) and plasma total GLP-1 concentrations during a standardized intraduodenal infusion of Glucose and 3-OMG in patients with type 2 diabetes. A total of 12 patients, treated with metformin 850 mg twice daily or placebo for 7 days each in a double-blind, randomized, crossover design (14 days' washout between treatments), were evaluated on days 5 or 8 of each treatment (6 subjects each). On each study day, 30 minutes after ingesting 850 mg metformin or placebo, patients received an infusion of Glucose (60 g + 5 g 3-OMG, dissolved in water to 240 mL) via an intraduodenal catheter over the course of 120 minutes. Compared with placebo, metformin was associated with lower serum 3-OMG ( P < .001) and higher plasma total GLP-1 ( P = .003) concentrations. The increment in plasma GLP-1 after metformin vs placebo was related to the reduction in serum 3-OMG concentrations ( P = .019). Accordingly, metformin inhibits small intestinal Glucose Absorption, which may contribute to augmented GLP-1 secretion in type 2 diabetes.
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accelerated intestinal Glucose Absorption in morbidly obese humans relationship to Glucose transporters incretin hormones and glycemia
The Journal of Clinical Endocrinology and Metabolism, 2015Co-Authors: Nam Q. Nguyen, Michael Horowitz, Christopher K Rayner, Adam M. Deane, Tamara L Debreceni, Jenna E Bambrick, Bridgette Chia, Judith M Wishart, Richard L YoungAbstract:CONTEXT: Intestinal Glucose Absorption is mediated by sodium-dependent Glucose transporter 1 (SGLT-1) and Glucose transporter 2 (GLUT2), which are linked to sweet taste receptor (STR) signaling and incretin responses. OBJECTIVE: This study aimed to examine intestinal Glucose Absorption in morbidly obese humans and its relationship to the expression of STR and Glucose transporters, glycemia, and incretin responses. DESIGN/SETTING/PARTICIPANTS: Seventeen nondiabetic, morbidly obese subjects (body mass index [BMI], 48 ± 4 kg/m(2)) and 11 lean controls (BMI, 25 ± 1 kg/m(2)) underwent endoscopic duodenal biopsies before and after a 30-minute intraduodenal Glucose infusion (30 g Glucose and 3 g 3-O-methylGlucose [3-OMG]). MAIN OUTCOME MEASURES: Blood Glucose and plasma concentrations of 3-OMG, Glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide 1 (GLP-1), insulin, and glucagon were measured over 270 minutes. Expression of duodenal SGLT-1, GLUT2, and STR (T1R2) was quantified by PCR. RESULTS: The increase in plasma 3-OMG (P < .001) and blood Glucose (P < .0001) were greater in obese than lean subjects. Plasma 3-OMG correlated directly with blood Glucose (r = 0.78, P < .01). In response to intraduodenal Glucose, plasma GIP (P < .001), glucagon (P < .001), and insulin (P < .001) were higher, but GLP-1 (P < .001) was less in the obese compared with lean. Expression of SGLT-1 (P = .035), but not GLUT2 or T1R2, was higher in the obese, and related to peak plasma 3-OMG (r = 0.60, P = .01), GIP (r = 0.67, P = .003), and insulin (r = 0.58, P = .02). CONCLUSIONS: In morbid obesity, proximal intestine Glucose Absorption is accelerated and related to increased SGLT-1 expression, leading to an incretin-glucagon profile promoting hyperinsulinemia and hyperglycemia. These findings are consistent with the concept that accelerated Glucose Absorption in the proximal gut underlies the foregut theory of obesity and type 2 diabetes.
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Glucose Absorption in small intestinal diseases
Expert review of gastroenterology & hepatology, 2014Co-Authors: Sony S. Thazhath, Richard L Young, Michael Horowitz, Christopher K RaynerAbstract:Recent developments in the field of diabetes and obesity management have established the central role of the gut in Glucose homeostasis; not only is the gut the primary absorptive site, but it also triggers neurohumoral feedback responses that regulate the pre- and postabsorptive phases of Glucose metabolism. Structural and/or functional disorders of the intestine have the capacity to enhance (eg: diabetes) or inhibit (eg: short-gut syndrome, critical illness) Glucose Absorption, with potentially detrimental outcomes. In this review, we first describe the normal physiology of Glucose Absorption and outline the methods by which it can be quantified. Then we focus on the structural and functional changes in the small intestine associated with obesity, critical illness, short gut syndrome and other malabsorptive states, and particularly Type 2 diabetes, which can impact upon carbohydrate Absorption and overall Glucose homeostasis.
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effect of the artificial sweetener sucralose on small intestinal Glucose Absorption in healthy human subjects
British Journal of Nutrition, 2010Co-Authors: Jessica Chang, Helen L Checklin, Richard L Young, Michael Horowitz, Karen L Jones, Christopher K RaynerAbstract:It has been reported that the artificial sweetener, sucralose, stimulates Glucose Absorption in rodents by enhancing apical availability of the transporter GLUT2. We evaluated whether exposure of the proximal small intestine to sucralose affects Glucose Absorption and/or the glycaemic response to an intraduodenal (ID) Glucose infusion in healthy human subjects. Ten healthy subjects were studied on two separate occasions in a single-blind, randomised order. Each subject received an ID infusion of sucralose (4 mM in 0.9 % saline) or control (0-9 % saline) at 4 ml/min for 150 min (T = - 30 to 120 min). After 30 min (T = 0), Glucose (25 %) and its non-metabolised analogue, 3-O-methylGlucose (3-OMG; 2.5 %), were co-infused intraduodenally (T= 0-120min; 4·2kJ/min (1 kcal/min)). Blood was sampled at frequent intervals. Blood Glucose, plasma glucagon-like peptide-1 (GLP-I) and serum 3-OMG concentrations increased during ID Glucose/3-OMG infusion (P<0·005 for each). However, there were no differences in blood Glucose, plasma GLP-1 or serum 3-OMG concentrations between sucralose and control infusions. In conclusion, sucralose does not appear to modify the rate of Glucose Absorption or the glycaemic or incretin response to ID Glucose infusion when given acutely in healthy human subjects.
Michael Horowitz - One of the best experts on this subject based on the ideXlab platform.
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Role of intestinal Glucose Absorption in Glucose tolerance.
Current opinion in pharmacology, 2020Co-Authors: Christopher K Rayner, Karen L Jones, Cong Xie, Chinmay S. Marathe, Michael HorowitzAbstract:Intestinal Glucose Absorption is integral to postprandial Glucose homeostasis. Glucose Absorption is dependent on a number of factors, including the exposure of carbohydrate to the mucosa of the upper gastrointestinal tract (determined particularly by the rates of gastric emptying and small intestinal transit), the digestion of complex carbohydrate into monosaccharides, and Glucose sensing and transport by the intestinal mucosa. The Absorption of Glucose in the small intestine is not only a determinant of the appearance of exogenous Glucose in the peripheral circulation, but is also coupled to the release of gastrointestinal hormones that in turn influence postprandial Glucose metabolism through modulating gastrointestinal motor function, insulin and glucagon secretion, and subsequent energy intake. This review describes the physiology and pathophysiology of intestinal Glucose Absorption in health and type 2 diabetes, including its relevance to Glucose tolerance and the management of postprandial hyperglycaemia.
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metformin reduces the rate of small intestinal Glucose Absorption in type 2 diabetes
Diabetes Obesity and Metabolism, 2017Co-Authors: Michael Horowitz, Karen L Jones, Cong Xie, Christopher K RaynerAbstract:In rodents, metformin slows intestinal Glucose Absorption, potentially increasing exposure of the distal gut to Glucose to enhance postprandial glucagon-like peptide-1 (GLP-1) secretion. We evaluated the effects of metformin on serum 3-O-methylGlucose (3-OMG; a marker of Glucose Absorption) and plasma total GLP-1 concentrations during a standardized intraduodenal infusion of Glucose and 3-OMG in patients with type 2 diabetes. A total of 12 patients, treated with metformin 850 mg twice daily or placebo for 7 days each in a double-blind, randomized, crossover design (14 days' washout between treatments), were evaluated on days 5 or 8 of each treatment (6 subjects each). On each study day, 30 minutes after ingesting 850 mg metformin or placebo, patients received an infusion of Glucose (60 g + 5 g 3-OMG, dissolved in water to 240 mL) via an intraduodenal catheter over the course of 120 minutes. Compared with placebo, metformin was associated with lower serum 3-OMG ( P < .001) and higher plasma total GLP-1 ( P = .003) concentrations. The increment in plasma GLP-1 after metformin vs placebo was related to the reduction in serum 3-OMG concentrations ( P = .019). Accordingly, metformin inhibits small intestinal Glucose Absorption, which may contribute to augmented GLP-1 secretion in type 2 diabetes.
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accelerated intestinal Glucose Absorption in morbidly obese humans relationship to Glucose transporters incretin hormones and glycemia
The Journal of Clinical Endocrinology and Metabolism, 2015Co-Authors: Nam Q. Nguyen, Michael Horowitz, Christopher K Rayner, Adam M. Deane, Tamara L Debreceni, Jenna E Bambrick, Bridgette Chia, Judith M Wishart, Richard L YoungAbstract:CONTEXT: Intestinal Glucose Absorption is mediated by sodium-dependent Glucose transporter 1 (SGLT-1) and Glucose transporter 2 (GLUT2), which are linked to sweet taste receptor (STR) signaling and incretin responses. OBJECTIVE: This study aimed to examine intestinal Glucose Absorption in morbidly obese humans and its relationship to the expression of STR and Glucose transporters, glycemia, and incretin responses. DESIGN/SETTING/PARTICIPANTS: Seventeen nondiabetic, morbidly obese subjects (body mass index [BMI], 48 ± 4 kg/m(2)) and 11 lean controls (BMI, 25 ± 1 kg/m(2)) underwent endoscopic duodenal biopsies before and after a 30-minute intraduodenal Glucose infusion (30 g Glucose and 3 g 3-O-methylGlucose [3-OMG]). MAIN OUTCOME MEASURES: Blood Glucose and plasma concentrations of 3-OMG, Glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide 1 (GLP-1), insulin, and glucagon were measured over 270 minutes. Expression of duodenal SGLT-1, GLUT2, and STR (T1R2) was quantified by PCR. RESULTS: The increase in plasma 3-OMG (P < .001) and blood Glucose (P < .0001) were greater in obese than lean subjects. Plasma 3-OMG correlated directly with blood Glucose (r = 0.78, P < .01). In response to intraduodenal Glucose, plasma GIP (P < .001), glucagon (P < .001), and insulin (P < .001) were higher, but GLP-1 (P < .001) was less in the obese compared with lean. Expression of SGLT-1 (P = .035), but not GLUT2 or T1R2, was higher in the obese, and related to peak plasma 3-OMG (r = 0.60, P = .01), GIP (r = 0.67, P = .003), and insulin (r = 0.58, P = .02). CONCLUSIONS: In morbid obesity, proximal intestine Glucose Absorption is accelerated and related to increased SGLT-1 expression, leading to an incretin-glucagon profile promoting hyperinsulinemia and hyperglycemia. These findings are consistent with the concept that accelerated Glucose Absorption in the proximal gut underlies the foregut theory of obesity and type 2 diabetes.
-
Glucose Absorption in small intestinal diseases
Expert review of gastroenterology & hepatology, 2014Co-Authors: Sony S. Thazhath, Richard L Young, Michael Horowitz, Christopher K RaynerAbstract:Recent developments in the field of diabetes and obesity management have established the central role of the gut in Glucose homeostasis; not only is the gut the primary absorptive site, but it also triggers neurohumoral feedback responses that regulate the pre- and postabsorptive phases of Glucose metabolism. Structural and/or functional disorders of the intestine have the capacity to enhance (eg: diabetes) or inhibit (eg: short-gut syndrome, critical illness) Glucose Absorption, with potentially detrimental outcomes. In this review, we first describe the normal physiology of Glucose Absorption and outline the methods by which it can be quantified. Then we focus on the structural and functional changes in the small intestine associated with obesity, critical illness, short gut syndrome and other malabsorptive states, and particularly Type 2 diabetes, which can impact upon carbohydrate Absorption and overall Glucose homeostasis.
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Glucose Absorption following gastric and small intestinal nutrient administration in the critically ill
Critical Care, 2011Co-Authors: Marianne J. Chapman, Laura K. Besanko, Adam M. Deane, A Di Bartolemeo, Antony V. Zaknic, Matthew J. Summers, Nam Q. Nguyen, Carly M. Burgstad, Michael HorowitzAbstract:Glucose Absorption from the stomach is abnormal related to slow gastric emptying and impaired in critically ill patients (CIP) with normal gastric emptying, suggesting that small intestinal (SI) factors may also be responsible. Small intestinal Absorption of nutrient has not been formally quantified in this group. The aim was to quantify and compare Glucose Absorption following gastric and SI administration in CIP and healthy volunteers (HV).
Richard L Young - One of the best experts on this subject based on the ideXlab platform.
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accelerated intestinal Glucose Absorption in morbidly obese humans relationship to Glucose transporters incretin hormones and glycemia
The Journal of Clinical Endocrinology and Metabolism, 2015Co-Authors: Nam Q. Nguyen, Michael Horowitz, Christopher K Rayner, Adam M. Deane, Tamara L Debreceni, Jenna E Bambrick, Bridgette Chia, Judith M Wishart, Richard L YoungAbstract:CONTEXT: Intestinal Glucose Absorption is mediated by sodium-dependent Glucose transporter 1 (SGLT-1) and Glucose transporter 2 (GLUT2), which are linked to sweet taste receptor (STR) signaling and incretin responses. OBJECTIVE: This study aimed to examine intestinal Glucose Absorption in morbidly obese humans and its relationship to the expression of STR and Glucose transporters, glycemia, and incretin responses. DESIGN/SETTING/PARTICIPANTS: Seventeen nondiabetic, morbidly obese subjects (body mass index [BMI], 48 ± 4 kg/m(2)) and 11 lean controls (BMI, 25 ± 1 kg/m(2)) underwent endoscopic duodenal biopsies before and after a 30-minute intraduodenal Glucose infusion (30 g Glucose and 3 g 3-O-methylGlucose [3-OMG]). MAIN OUTCOME MEASURES: Blood Glucose and plasma concentrations of 3-OMG, Glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide 1 (GLP-1), insulin, and glucagon were measured over 270 minutes. Expression of duodenal SGLT-1, GLUT2, and STR (T1R2) was quantified by PCR. RESULTS: The increase in plasma 3-OMG (P < .001) and blood Glucose (P < .0001) were greater in obese than lean subjects. Plasma 3-OMG correlated directly with blood Glucose (r = 0.78, P < .01). In response to intraduodenal Glucose, plasma GIP (P < .001), glucagon (P < .001), and insulin (P < .001) were higher, but GLP-1 (P < .001) was less in the obese compared with lean. Expression of SGLT-1 (P = .035), but not GLUT2 or T1R2, was higher in the obese, and related to peak plasma 3-OMG (r = 0.60, P = .01), GIP (r = 0.67, P = .003), and insulin (r = 0.58, P = .02). CONCLUSIONS: In morbid obesity, proximal intestine Glucose Absorption is accelerated and related to increased SGLT-1 expression, leading to an incretin-glucagon profile promoting hyperinsulinemia and hyperglycemia. These findings are consistent with the concept that accelerated Glucose Absorption in the proximal gut underlies the foregut theory of obesity and type 2 diabetes.
-
Glucose Absorption in small intestinal diseases
Expert review of gastroenterology & hepatology, 2014Co-Authors: Sony S. Thazhath, Richard L Young, Michael Horowitz, Christopher K RaynerAbstract:Recent developments in the field of diabetes and obesity management have established the central role of the gut in Glucose homeostasis; not only is the gut the primary absorptive site, but it also triggers neurohumoral feedback responses that regulate the pre- and postabsorptive phases of Glucose metabolism. Structural and/or functional disorders of the intestine have the capacity to enhance (eg: diabetes) or inhibit (eg: short-gut syndrome, critical illness) Glucose Absorption, with potentially detrimental outcomes. In this review, we first describe the normal physiology of Glucose Absorption and outline the methods by which it can be quantified. Then we focus on the structural and functional changes in the small intestine associated with obesity, critical illness, short gut syndrome and other malabsorptive states, and particularly Type 2 diabetes, which can impact upon carbohydrate Absorption and overall Glucose homeostasis.
-
effect of the artificial sweetener sucralose on small intestinal Glucose Absorption in healthy human subjects
British Journal of Nutrition, 2010Co-Authors: Jessica Chang, Helen L Checklin, Richard L Young, Michael Horowitz, Karen L Jones, Christopher K RaynerAbstract:It has been reported that the artificial sweetener, sucralose, stimulates Glucose Absorption in rodents by enhancing apical availability of the transporter GLUT2. We evaluated whether exposure of the proximal small intestine to sucralose affects Glucose Absorption and/or the glycaemic response to an intraduodenal (ID) Glucose infusion in healthy human subjects. Ten healthy subjects were studied on two separate occasions in a single-blind, randomised order. Each subject received an ID infusion of sucralose (4 mM in 0.9 % saline) or control (0-9 % saline) at 4 ml/min for 150 min (T = - 30 to 120 min). After 30 min (T = 0), Glucose (25 %) and its non-metabolised analogue, 3-O-methylGlucose (3-OMG; 2.5 %), were co-infused intraduodenally (T= 0-120min; 4·2kJ/min (1 kcal/min)). Blood was sampled at frequent intervals. Blood Glucose, plasma glucagon-like peptide-1 (GLP-I) and serum 3-OMG concentrations increased during ID Glucose/3-OMG infusion (P<0·005 for each). However, there were no differences in blood Glucose, plasma GLP-1 or serum 3-OMG concentrations between sucralose and control infusions. In conclusion, sucralose does not appear to modify the rate of Glucose Absorption or the glycaemic or incretin response to ID Glucose infusion when given acutely in healthy human subjects.
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effect of the artificial sweetener sucralose on small intestinal Glucose Absorption in healthy human subjects
British Journal of Nutrition, 2010Co-Authors: Jessica Chang, Helen L Checklin, Richard L Young, Michael Horowitz, Karen L Jones, Christopher K RaynerAbstract:It has been reported that the artificial sweetener, sucralose, stimulates Glucose Absorption in rodents by enhancing apical availability of the transporter GLUT2. We evaluated whether exposure of the proximal small intestine to sucralose affects Glucose Absorption and/or the glycaemic response to an intraduodenal (ID) Glucose infusion in healthy human subjects. Ten healthy subjects were studied on two separate occasions in a single-blind, randomised order. Each subject received an ID infusion of sucralose (4 mM in 0.9 % saline) or control (0-9 % saline) at 4 ml/min for 150 min (T = - 30 to 120 min). After 30 min (T = 0), Glucose (25 %) and its non-metabolised analogue, 3-O-methylGlucose (3-OMG; 2.5 %), were co-infused intraduodenally (T= 0-120min; 4·2kJ/min (1 kcal/min)). Blood was sampled at frequent intervals. Blood Glucose, plasma glucagon-like peptide-1 (GLP-I) and serum 3-OMG concentrations increased during ID Glucose/3-OMG infusion (P<0·005 for each). However, there were no differences in blood Glucose, plasma GLP-1 or serum 3-OMG concentrations between sucralose and control infusions. In conclusion, sucralose does not appear to modify the rate of Glucose Absorption or the glycaemic or incretin response to ID Glucose infusion when given acutely in healthy human subjects.
Karen L Jones - One of the best experts on this subject based on the ideXlab platform.
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Role of intestinal Glucose Absorption in Glucose tolerance.
Current opinion in pharmacology, 2020Co-Authors: Christopher K Rayner, Karen L Jones, Cong Xie, Chinmay S. Marathe, Michael HorowitzAbstract:Intestinal Glucose Absorption is integral to postprandial Glucose homeostasis. Glucose Absorption is dependent on a number of factors, including the exposure of carbohydrate to the mucosa of the upper gastrointestinal tract (determined particularly by the rates of gastric emptying and small intestinal transit), the digestion of complex carbohydrate into monosaccharides, and Glucose sensing and transport by the intestinal mucosa. The Absorption of Glucose in the small intestine is not only a determinant of the appearance of exogenous Glucose in the peripheral circulation, but is also coupled to the release of gastrointestinal hormones that in turn influence postprandial Glucose metabolism through modulating gastrointestinal motor function, insulin and glucagon secretion, and subsequent energy intake. This review describes the physiology and pathophysiology of intestinal Glucose Absorption in health and type 2 diabetes, including its relevance to Glucose tolerance and the management of postprandial hyperglycaemia.
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metformin reduces the rate of small intestinal Glucose Absorption in type 2 diabetes
Diabetes Obesity and Metabolism, 2017Co-Authors: Michael Horowitz, Karen L Jones, Cong Xie, Christopher K RaynerAbstract:In rodents, metformin slows intestinal Glucose Absorption, potentially increasing exposure of the distal gut to Glucose to enhance postprandial glucagon-like peptide-1 (GLP-1) secretion. We evaluated the effects of metformin on serum 3-O-methylGlucose (3-OMG; a marker of Glucose Absorption) and plasma total GLP-1 concentrations during a standardized intraduodenal infusion of Glucose and 3-OMG in patients with type 2 diabetes. A total of 12 patients, treated with metformin 850 mg twice daily or placebo for 7 days each in a double-blind, randomized, crossover design (14 days' washout between treatments), were evaluated on days 5 or 8 of each treatment (6 subjects each). On each study day, 30 minutes after ingesting 850 mg metformin or placebo, patients received an infusion of Glucose (60 g + 5 g 3-OMG, dissolved in water to 240 mL) via an intraduodenal catheter over the course of 120 minutes. Compared with placebo, metformin was associated with lower serum 3-OMG ( P < .001) and higher plasma total GLP-1 ( P = .003) concentrations. The increment in plasma GLP-1 after metformin vs placebo was related to the reduction in serum 3-OMG concentrations ( P = .019). Accordingly, metformin inhibits small intestinal Glucose Absorption, which may contribute to augmented GLP-1 secretion in type 2 diabetes.
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effect of the artificial sweetener sucralose on small intestinal Glucose Absorption in healthy human subjects
British Journal of Nutrition, 2010Co-Authors: Jessica Chang, Helen L Checklin, Richard L Young, Michael Horowitz, Karen L Jones, Christopher K RaynerAbstract:It has been reported that the artificial sweetener, sucralose, stimulates Glucose Absorption in rodents by enhancing apical availability of the transporter GLUT2. We evaluated whether exposure of the proximal small intestine to sucralose affects Glucose Absorption and/or the glycaemic response to an intraduodenal (ID) Glucose infusion in healthy human subjects. Ten healthy subjects were studied on two separate occasions in a single-blind, randomised order. Each subject received an ID infusion of sucralose (4 mM in 0.9 % saline) or control (0-9 % saline) at 4 ml/min for 150 min (T = - 30 to 120 min). After 30 min (T = 0), Glucose (25 %) and its non-metabolised analogue, 3-O-methylGlucose (3-OMG; 2.5 %), were co-infused intraduodenally (T= 0-120min; 4·2kJ/min (1 kcal/min)). Blood was sampled at frequent intervals. Blood Glucose, plasma glucagon-like peptide-1 (GLP-I) and serum 3-OMG concentrations increased during ID Glucose/3-OMG infusion (P<0·005 for each). However, there were no differences in blood Glucose, plasma GLP-1 or serum 3-OMG concentrations between sucralose and control infusions. In conclusion, sucralose does not appear to modify the rate of Glucose Absorption or the glycaemic or incretin response to ID Glucose infusion when given acutely in healthy human subjects.
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effect of the artificial sweetener sucralose on small intestinal Glucose Absorption in healthy human subjects
British Journal of Nutrition, 2010Co-Authors: Jessica Chang, Helen L Checklin, Richard L Young, Michael Horowitz, Karen L Jones, Christopher K RaynerAbstract:It has been reported that the artificial sweetener, sucralose, stimulates Glucose Absorption in rodents by enhancing apical availability of the transporter GLUT2. We evaluated whether exposure of the proximal small intestine to sucralose affects Glucose Absorption and/or the glycaemic response to an intraduodenal (ID) Glucose infusion in healthy human subjects. Ten healthy subjects were studied on two separate occasions in a single-blind, randomised order. Each subject received an ID infusion of sucralose (4 mM in 0.9 % saline) or control (0-9 % saline) at 4 ml/min for 150 min (T = - 30 to 120 min). After 30 min (T = 0), Glucose (25 %) and its non-metabolised analogue, 3-O-methylGlucose (3-OMG; 2.5 %), were co-infused intraduodenally (T= 0-120min; 4·2kJ/min (1 kcal/min)). Blood was sampled at frequent intervals. Blood Glucose, plasma glucagon-like peptide-1 (GLP-I) and serum 3-OMG concentrations increased during ID Glucose/3-OMG infusion (P<0·005 for each). However, there were no differences in blood Glucose, plasma GLP-1 or serum 3-OMG concentrations between sucralose and control infusions. In conclusion, sucralose does not appear to modify the rate of Glucose Absorption or the glycaemic or incretin response to ID Glucose infusion when given acutely in healthy human subjects.
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Glucose Absorption and gastric emptying in critical illness
Critical care (London England), 2009Co-Authors: Marianne J. Chapman, Karen L Jones, Robert J. Fraser, Geoffrey M. Matthews, Antonietta Russo, Max Bellon, Laura K. Besanko, Ross N. Butler, Barry E. Chatterton, Michael HorowitzAbstract:Delayed gastric emptying occurs frequently in critically ill patients and has the potential to adversely affect both the rate, and extent, of nutrient Absorption. However, there is limited information about nutrient Absorption in the critically ill, and the relationship between gastric emptying (GE) and Absorption has hitherto not been evaluated. The aim of this study was to quantify Glucose Absorption and the relationships between GE, Glucose Absorption and glycaemia in critically ill patients. Studies were performed in nineteen mechanically-ventilated critically ill patients and compared to nineteen healthy subjects. Following 4 hours fasting, 100 ml of Ensure, 2 g 3-O-methyl Glucose (3-OMG) and 99mTc sulphur colloid were infused into the stomach over 5 minutes. Glucose Absorption (plasma 3-OMG), blood Glucose levels and GE (scintigraphy) were measured over four hours. Data are mean ± SEM. A P-value 0.51; P < 0.05). In critically ill patients; (i) the rate and extent of Glucose Absorption are markedly reduced; (ii) GE is a major determinant of the rate of Absorption, but does not fully account for the extent of impaired Absorption; (iii) blood Glucose concentration could be one of a number of factors affecting GE.
Chaivat Toskulkao - One of the best experts on this subject based on the ideXlab platform.
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Effects of Stevioside and Steviol on Intestinal Glucose Absorption in Hamsters
Journal of Nutritional Science and Vitaminology, 1995Co-Authors: Chaivat Toskulkao, Monthaporn Sutheerawatananon, Chaitip Wanichanon, Porncharn Saitongdee, Maitree SuttajitAbstract:The effects of stevioside and steviol (a product of enzy-matic hydrolysis of stevioside) on intestinal Glucose Absorption were examined in the hamster jejunum in vitro. By using the jejunal rings technique, we found that stevioside at a high dose of 5 mM had no inhibitory effect on Glucose Absorption. In contrast, Glucose Absorption was inhibited 43% by 1 mM steviol. The inhibition of Glucose Absorption by steviol was related to steviol concentration and incubation time. The inhibitory effect of steviol compared to phlorizin and ouabain was also investigated. Steviol, which caused a decrease in Glucose accumulation in the intestinal ring tissues, possibly acts on the brush border membrane as does phlorizin. Furthermore, it was also found that steviol altered the morphology of the intestinal absorptive cells. These results suggest that the possible site of inhibitory action of steviol might be on the mucosal side and/or at the intracellular organelles of intestinal absorptive cells.
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Inhibitory effect of steviol, a metabolite of stevioside, on Glucose Absorption in everted hamster intestine in vitro
Toxicology letters, 1995Co-Authors: Chaivat Toskulkao, Monthaporn Sutheerawattananon, Pawinee PiyachaturawatAbstract:The effects of stevioside and steviol (a product of enzymatic hydrolysis of stevioside) on intestinal Glucose Absorption were examined in hamster jejunum. By using the everted sac technique, we found that stevioside (1 and 5 mM) had no inhibitory effect on Glucose Absorption. In contrast, Glucose Absorption was inhibited 29% by 1 mM steviol. The inhibition of Glucose Absorption by steviol was related to steviol concentration and incubation time. The possible mechanism of steviol inhibitory action of Glucose Absorption was also investigated. Reductions in the intestinal mucosal ATP content and absorptive surface area were responsible for the inhibition of Glucose Absorption by steviol. The decrease in the intestinal mucosal ATP content was accompanied by a decrease in the activities of mitochondrial NADH cytochrome c reductase and cytochrome oxidase. Moreover, no inhibitory effects of steviol on the activity of intestinal Na+,K(+)-ATPase and Glucose uptake in the intestinal brush-border membrane vesicles were seen. These results suggest that inhibition of intestinal Glucose Absorption by steviol in hamsters is due to the reduction in mucosal ATP content and an alteration of the morphology of the intestinal absorptive cells.
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Effects of stevioside, a natural sweetener, on intestinal Glucose Absorption in hamsters
Nutrition Research, 1994Co-Authors: Chaivat Toskulkao, Monthaporn SutheerawattananonAbstract:Abstract Effects of stevioside, a natural sweetener, on intestinal Glucose Absorption were examined in hamsters. Oral administration by gavage of a high dose of stevioside at 2.5 g/kg BW/day for 12 weeks caused inhibition of Glucose Absorption, but lower doses of 0.5 and 1 g/kg BW/day had no effect. Reductions in the activity of intestinal Na + −K + -ATPase and absorptive surface area were responsible for the inhibition of Glucose Absorption by stevioside. In addition, stevioside at a dose of 2.5 g/kg BW/day for 12 weeks also caused a reduction in body weight and an increase in sucrase activity of the jejunum. These results suggest that inhibition of Glucose Absorption by stevioside in hamsters is due to the inhibition of intestinal mucosal Na + −K + -ATPase and an alteration of the morphology of the intestinal absorptive cells which would lead to reductions in body weight of hamsters.