The Experts below are selected from a list of 222 Experts worldwide ranked by ideXlab platform
Michael Horowitz - One of the best experts on this subject based on the ideXlab platform.
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Hypoglycaemia and Gastric Emptying
Diabetes obesity & metabolism, 2018Co-Authors: Chinmay S. Marathe, Jessica A. Marathe, Christopher K. Rayner, Palash Kar, Karen L. Jones, Michael HorowitzAbstract:Hypoglycaemia is arguably the most important complication of insulin therapy in type 1 and type 2 diabetes. Counter-regulation of hypoglycaemia is dependent on autonomic function and frequent hypoglycaemia may lead to reductions in both autonomic warning signals and the catecholamine response, the so-called "impaired awareness of hypoglycaemia". It is now appreciated that Gastric Emptying is a major determinant of the glycaemic response to carbohydrate-containing meals in both health and diabetes, that disordered (especially delayed) Gastric Emptying occurs frequently in diabetes, and that acute hypoglycaemia accelerates Gastric Emptying substantially. However, the potential relevance of Gastric Emptying to the predisposition to, and counter-regulation of, hypoglycaemia has received little attention. In insulin-treated patients, the rate of Gastric Emptying influences the timing of the postprandial insulin requirement, and gastroparesis is likely to predispose to postprandial hypoglycaemia. Conversely, the marked acceleration of Gastric Emptying induced by hypoglycaemia probably represents an important counter-regulatory response to increase the rate of carbohydrate absorption. This review summarizes the current knowledge of the inter-relationships between hypoglycaemia and Gastric Emptying, with a focus on clinical implications.
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Gastric Emptying and glycaemia in health and diabetes mellitus
Nature Reviews Endocrinology, 2015Co-Authors: Liza K. Phillips, Christopher K. Rayner, Karen L. Jones, Adam M. Deane, Michael HorowitzAbstract:The rate of Gastric Emptying is a critical determinant of postprandial glycaemia and, accordingly, is fundamental to maintaining blood glucose homeostasis. Disordered Gastric Emptying occurs frequently in patients with longstanding type 1 diabetes mellitus and type 2 diabetes mellitus (T2DM). A complex bidirectional relationship exists between Gastric Emptying and glycaemia—Gastric Emptying accounts for ∼35% of the variance in peak postprandial blood glucose concentrations in healthy individuals and in patients with diabetes mellitus, and the rate of Emptying is itself modulated by acute changes in glycaemia. Clinical implementation of incretin-based therapies for the management of T2DM, which diminish postprandial glycaemia, in part by slowing Gastric Emptying, is widespread. Other therapies for patients with T2DM, which specifically target Gastric Emptying include pramlintide and dietary-based treatment approaches. A weak association exists between upper gastrointestinal symptoms and the rate of Gastric Emptying. In patients with severe diabetic gastroparesis, pathological changes are highly variable and are characterized by loss of interstitial cells of Cajal and an immune infiltrate. Management options for patients with symptomatic gastroparesis remain limited in their efficacy, which probably reflects the heterogeneous nature of the underlying pathophysiology. The rate of Gastric Emptying is a critical determinant of postprandial glycaemia Disordered Gastric Emptying is common in patients with longstanding type 1 diabetes mellitus and type 2 diabetes mellitus; however, the prevalence and natural history of diabetic gastroparesis is poorly defined A number of management strategies for patients with type 2 diabetes mellitus specifically target Gastric Emptying A bidirectional relationship exists between the rate of Gastric Emptying and glycaemia, such that the rate of Gastric Emptying is partially modulated by acute changes in blood glucose concentrations In patients with severe diabetic gastroparesis, histological abnormalities are heterogeneous; however, presence of an immune infiltrate and loss of interstitial cells of Cajal are evident in the majority of patients Currently available management strategies for symptomatic diabetic gastroparesis have limited efficacy and further work in this area is required Disordered Gastric Emptying (also known as gastroparesis) is a complication frequently associated with long-standing type 1 diabetes mellitus and type 2 diabetes mellitus. In this Review, Phillips and colleagues discuss the underlying pathophysiology of gastroparesis in patients with diabetes mellitus. In addition, diagnosis, symptom management and emerging therapies are addressed.
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Gastric Emptying and glycaemia in health and diabetes mellitus
Nature reviews. Endocrinology, 2014Co-Authors: Liza K. Phillips, Christopher K. Rayner, Karen L. Jones, Adam M. Deane, Michael HorowitzAbstract:The rate of Gastric Emptying is a critical determinant of postprandial glycaemia and, accordingly, is fundamental to maintaining blood glucose homeostasis. Disordered Gastric Emptying occurs frequently in patients with longstanding type 1 diabetes mellitus and type 2 diabetes mellitus (T2DM). A complex bidirectional relationship exists between Gastric Emptying and glycaemia--Gastric Emptying accounts for ∼35% of the variance in peak postprandial blood glucose concentrations in healthy individuals and in patients with diabetes mellitus, and the rate of Emptying is itself modulated by acute changes in glycaemia. Clinical implementation of incretin-based therapies for the management of T2DM, which diminish postprandial glycaemia, in part by slowing Gastric Emptying, is widespread. Other therapies for patients with T2DM, which specifically target Gastric Emptying include pramlintide and dietary-based treatment approaches. A weak association exists between upper gastrointestinal symptoms and the rate of Gastric Emptying. In patients with severe diabetic gastroparesis, pathological changes are highly variable and are characterized by loss of interstitial cells of Cajal and an immune infiltrate. Management options for patients with symptomatic gastroparesis remain limited in their efficacy, which probably reflects the heterogeneous nature of the underlying pathophysiology.
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Measurement of Gastric Emptying in diabetes
Journal of diabetes and its complications, 2014Co-Authors: Liza K. Phillips, Christopher K. Rayner, Karen L. Jones, Michael HorowitzAbstract:Abstract There has been a substantial evolution of concepts related to disordered Gastric Emptying in diabetes. While the traditional focus has hitherto related to the pathophysiology and management of upper gastrointestinal symptoms associated with gastroparesis, it is now apparent that the rate of Gastric Emptying is central to the regulation of postprandial glycemia. This recognition has stimulated the development of dietary and pharmacologic approaches to optimize glycemic control, at least in part, by slowing Gastric Emptying. With the increased clinical interest in this area, it has proved necessary to expand the traditional indications for Gastric Emptying studies, and consider the relative strengths and limitations of available techniques. Scintigraphy remains the ‘gold standard’ for the measurement of Gastric Emptying, however, there is a lack of standardization of the technique, and the optimal test meal for the evaluation of gastrointestinal symptoms may be discordant from that which is optimal to assess impaired glycemic control. The stable isotope breath test provides an alternative to scintigraphy and can be performed in an office-based setting. The effect of glucagon-like peptide-1 (GLP-1) and its agonists to reduce postprandial glycemia is dependent on the baseline rate of Gastric Emptying, as well as the magnitude of slowing. Because the effect of exogenous GLP-1 to slow Gastric Emptying is subject to tachyphylaxis with sustained receptor exposure, ‘short acting’ or ‘prandial’ GLP-1 agonists primarily target postprandial glycemia through slowing of Gastric Emptying, while ‘long acting’ or ‘non-prandial’ agents lower fasting glucose primarily through insulinotropic and glucagonostatic mechanisms. Accordingly, the indications for the therapeutic use of these different agents are likely to vary according to baseline Gastric Emptying rate and glycemic profiles.
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Predictors of Delayed Gastric Emptying in Diabetes
Diabetes care, 2001Co-Authors: Karen L. Jones, Judith M. Wishart, Antonietta Russo, Julie E. Stevens, Melanie K. Berry, Michael HorowitzAbstract:OBJECTIVE —To define the predictors of the rate of Gastric Emptying in patients with diabetes. RESEARCH DESIGN AND METHODS —A total of 101 outpatients with diabetes (79 type 1 and 22 type 2) underwent measurements of Gastric Emptying of a solid/liquid meal (scintigraphy), upper gastrointestinal symptoms (questionnaire), glycemic control (blood glucose concentrations during Gastric Emptying measurement), and autonomic nerve function (cardiovascular reflexes). RESULTS —The Gastric Emptying of solid and/or liquid was delayed in 66 (65%) patients. Solid (retention at 100 min 64 ± 3.2 vs. 50.2 ± 3.6%, P P P CONCLUSIONS —We conclude that the presence of abdominal bloating/fullness but not any other upper gastrointestinal symptom is associated with diabetic gastroparesis and that Gastric Emptying is slower in diabetic women than in diabetic men.
Christopher K. Rayner - One of the best experts on this subject based on the ideXlab platform.
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Hypoglycaemia and Gastric Emptying
Diabetes obesity & metabolism, 2018Co-Authors: Chinmay S. Marathe, Jessica A. Marathe, Christopher K. Rayner, Palash Kar, Karen L. Jones, Michael HorowitzAbstract:Hypoglycaemia is arguably the most important complication of insulin therapy in type 1 and type 2 diabetes. Counter-regulation of hypoglycaemia is dependent on autonomic function and frequent hypoglycaemia may lead to reductions in both autonomic warning signals and the catecholamine response, the so-called "impaired awareness of hypoglycaemia". It is now appreciated that Gastric Emptying is a major determinant of the glycaemic response to carbohydrate-containing meals in both health and diabetes, that disordered (especially delayed) Gastric Emptying occurs frequently in diabetes, and that acute hypoglycaemia accelerates Gastric Emptying substantially. However, the potential relevance of Gastric Emptying to the predisposition to, and counter-regulation of, hypoglycaemia has received little attention. In insulin-treated patients, the rate of Gastric Emptying influences the timing of the postprandial insulin requirement, and gastroparesis is likely to predispose to postprandial hypoglycaemia. Conversely, the marked acceleration of Gastric Emptying induced by hypoglycaemia probably represents an important counter-regulatory response to increase the rate of carbohydrate absorption. This review summarizes the current knowledge of the inter-relationships between hypoglycaemia and Gastric Emptying, with a focus on clinical implications.
-
Gastric Emptying and glycaemia in health and diabetes mellitus
Nature Reviews Endocrinology, 2015Co-Authors: Liza K. Phillips, Christopher K. Rayner, Karen L. Jones, Adam M. Deane, Michael HorowitzAbstract:The rate of Gastric Emptying is a critical determinant of postprandial glycaemia and, accordingly, is fundamental to maintaining blood glucose homeostasis. Disordered Gastric Emptying occurs frequently in patients with longstanding type 1 diabetes mellitus and type 2 diabetes mellitus (T2DM). A complex bidirectional relationship exists between Gastric Emptying and glycaemia—Gastric Emptying accounts for ∼35% of the variance in peak postprandial blood glucose concentrations in healthy individuals and in patients with diabetes mellitus, and the rate of Emptying is itself modulated by acute changes in glycaemia. Clinical implementation of incretin-based therapies for the management of T2DM, which diminish postprandial glycaemia, in part by slowing Gastric Emptying, is widespread. Other therapies for patients with T2DM, which specifically target Gastric Emptying include pramlintide and dietary-based treatment approaches. A weak association exists between upper gastrointestinal symptoms and the rate of Gastric Emptying. In patients with severe diabetic gastroparesis, pathological changes are highly variable and are characterized by loss of interstitial cells of Cajal and an immune infiltrate. Management options for patients with symptomatic gastroparesis remain limited in their efficacy, which probably reflects the heterogeneous nature of the underlying pathophysiology. The rate of Gastric Emptying is a critical determinant of postprandial glycaemia Disordered Gastric Emptying is common in patients with longstanding type 1 diabetes mellitus and type 2 diabetes mellitus; however, the prevalence and natural history of diabetic gastroparesis is poorly defined A number of management strategies for patients with type 2 diabetes mellitus specifically target Gastric Emptying A bidirectional relationship exists between the rate of Gastric Emptying and glycaemia, such that the rate of Gastric Emptying is partially modulated by acute changes in blood glucose concentrations In patients with severe diabetic gastroparesis, histological abnormalities are heterogeneous; however, presence of an immune infiltrate and loss of interstitial cells of Cajal are evident in the majority of patients Currently available management strategies for symptomatic diabetic gastroparesis have limited efficacy and further work in this area is required Disordered Gastric Emptying (also known as gastroparesis) is a complication frequently associated with long-standing type 1 diabetes mellitus and type 2 diabetes mellitus. In this Review, Phillips and colleagues discuss the underlying pathophysiology of gastroparesis in patients with diabetes mellitus. In addition, diagnosis, symptom management and emerging therapies are addressed.
-
Gastric Emptying and glycaemia in health and diabetes mellitus
Nature reviews. Endocrinology, 2014Co-Authors: Liza K. Phillips, Christopher K. Rayner, Karen L. Jones, Adam M. Deane, Michael HorowitzAbstract:The rate of Gastric Emptying is a critical determinant of postprandial glycaemia and, accordingly, is fundamental to maintaining blood glucose homeostasis. Disordered Gastric Emptying occurs frequently in patients with longstanding type 1 diabetes mellitus and type 2 diabetes mellitus (T2DM). A complex bidirectional relationship exists between Gastric Emptying and glycaemia--Gastric Emptying accounts for ∼35% of the variance in peak postprandial blood glucose concentrations in healthy individuals and in patients with diabetes mellitus, and the rate of Emptying is itself modulated by acute changes in glycaemia. Clinical implementation of incretin-based therapies for the management of T2DM, which diminish postprandial glycaemia, in part by slowing Gastric Emptying, is widespread. Other therapies for patients with T2DM, which specifically target Gastric Emptying include pramlintide and dietary-based treatment approaches. A weak association exists between upper gastrointestinal symptoms and the rate of Gastric Emptying. In patients with severe diabetic gastroparesis, pathological changes are highly variable and are characterized by loss of interstitial cells of Cajal and an immune infiltrate. Management options for patients with symptomatic gastroparesis remain limited in their efficacy, which probably reflects the heterogeneous nature of the underlying pathophysiology.
-
Measurement of Gastric Emptying in diabetes
Journal of diabetes and its complications, 2014Co-Authors: Liza K. Phillips, Christopher K. Rayner, Karen L. Jones, Michael HorowitzAbstract:Abstract There has been a substantial evolution of concepts related to disordered Gastric Emptying in diabetes. While the traditional focus has hitherto related to the pathophysiology and management of upper gastrointestinal symptoms associated with gastroparesis, it is now apparent that the rate of Gastric Emptying is central to the regulation of postprandial glycemia. This recognition has stimulated the development of dietary and pharmacologic approaches to optimize glycemic control, at least in part, by slowing Gastric Emptying. With the increased clinical interest in this area, it has proved necessary to expand the traditional indications for Gastric Emptying studies, and consider the relative strengths and limitations of available techniques. Scintigraphy remains the ‘gold standard’ for the measurement of Gastric Emptying, however, there is a lack of standardization of the technique, and the optimal test meal for the evaluation of gastrointestinal symptoms may be discordant from that which is optimal to assess impaired glycemic control. The stable isotope breath test provides an alternative to scintigraphy and can be performed in an office-based setting. The effect of glucagon-like peptide-1 (GLP-1) and its agonists to reduce postprandial glycemia is dependent on the baseline rate of Gastric Emptying, as well as the magnitude of slowing. Because the effect of exogenous GLP-1 to slow Gastric Emptying is subject to tachyphylaxis with sustained receptor exposure, ‘short acting’ or ‘prandial’ GLP-1 agonists primarily target postprandial glycemia through slowing of Gastric Emptying, while ‘long acting’ or ‘non-prandial’ agents lower fasting glucose primarily through insulinotropic and glucagonostatic mechanisms. Accordingly, the indications for the therapeutic use of these different agents are likely to vary according to baseline Gastric Emptying rate and glycemic profiles.
Daniel Sifrim - One of the best experts on this subject based on the ideXlab platform.
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Gastroesophageal reflux and Gastric Emptying: An update
Current GERD Reports, 2007Co-Authors: Sara Emerenziani, Daniel SifrimAbstract:In healthy subjects and patients with gastroesophageal reflux disease (GERD), most gastroesophageal reflux events occur during the postprandial period, suggesting a relationship between the volume and characteristics of the Gastric contents and the likelihood of reflux. Different techniques have been developed to characterize the dynamics of Gastric Emptying, including scintigraphy, octanoic acid breath tests, ultrasound, and more recently MRI. Although a delayed Gastric Emptying increasing gastroesophageal reflux by increasing the availability of material to reflux or by inducing prolonged Gastric distension and more transient lower esophageal sphincter relaxations may seem logical, the pathogenic role of delayed Gastric Emptying in GERD remains controversial. This is because several studies failed to demonstrate a correlation between abnormalities in Gastric Emptying and GERD symptoms or severity of esophagitis. Furthermore, treatment of GERD with Gastric prokinetic drugs has been disappointing. This review discusses the relationship between gastroesophageal reflux and Gastric Emptying of the whole stomach, the role of postprandial intraGastric distribution and Emptying of the proximal stomach, and a new hypothesis concerning the effect of Gastric Emptying, mixing, and buffering capacity of a meal on the frequency and acidity of refluxate.
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Gastroesophageal reflux and Gastric Emptying, revisited.
Current gastroenterology reports, 2005Co-Authors: Sara Emerenziani, Daniel SifrimAbstract:Total Gastric Emptying is delayed in 10% to 33% of adult patients with gastroesophageal reflux disease (GERD), but a strong correlation between duration of Gastric Emptying and severity of acid reflux or esophagitis has never been proved. Previous studies reported that patients with GERD might have exaggerated postprandial fundus relaxation with retention of food and triggering of transient lower esophageal sphincter relaxations (TLESRs). There is a positive correlation between postprandial fundus relaxation and number of TLESRs and also between proximal Gastric Emptying and esophageal acid exposure. However, new studies suggest that a high number of TLESRs and reflux events may occur even with accelerated Gastric Emptying, and prolonged Gastric retention might be associated with less rather than more esophageal acid exposure. Using simultaneous Gastric Emptying and esophageal pH impedance we found that the rate of Gastric Emptying might determine the acidity and proximal extent of reflux: The slower the Emptying, the higher the pH and proximal extent of the refluxate.
Karen L. Jones - One of the best experts on this subject based on the ideXlab platform.
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Hypoglycaemia and Gastric Emptying
Diabetes obesity & metabolism, 2018Co-Authors: Chinmay S. Marathe, Jessica A. Marathe, Christopher K. Rayner, Palash Kar, Karen L. Jones, Michael HorowitzAbstract:Hypoglycaemia is arguably the most important complication of insulin therapy in type 1 and type 2 diabetes. Counter-regulation of hypoglycaemia is dependent on autonomic function and frequent hypoglycaemia may lead to reductions in both autonomic warning signals and the catecholamine response, the so-called "impaired awareness of hypoglycaemia". It is now appreciated that Gastric Emptying is a major determinant of the glycaemic response to carbohydrate-containing meals in both health and diabetes, that disordered (especially delayed) Gastric Emptying occurs frequently in diabetes, and that acute hypoglycaemia accelerates Gastric Emptying substantially. However, the potential relevance of Gastric Emptying to the predisposition to, and counter-regulation of, hypoglycaemia has received little attention. In insulin-treated patients, the rate of Gastric Emptying influences the timing of the postprandial insulin requirement, and gastroparesis is likely to predispose to postprandial hypoglycaemia. Conversely, the marked acceleration of Gastric Emptying induced by hypoglycaemia probably represents an important counter-regulatory response to increase the rate of carbohydrate absorption. This review summarizes the current knowledge of the inter-relationships between hypoglycaemia and Gastric Emptying, with a focus on clinical implications.
-
Gastric Emptying and glycaemia in health and diabetes mellitus
Nature Reviews Endocrinology, 2015Co-Authors: Liza K. Phillips, Christopher K. Rayner, Karen L. Jones, Adam M. Deane, Michael HorowitzAbstract:The rate of Gastric Emptying is a critical determinant of postprandial glycaemia and, accordingly, is fundamental to maintaining blood glucose homeostasis. Disordered Gastric Emptying occurs frequently in patients with longstanding type 1 diabetes mellitus and type 2 diabetes mellitus (T2DM). A complex bidirectional relationship exists between Gastric Emptying and glycaemia—Gastric Emptying accounts for ∼35% of the variance in peak postprandial blood glucose concentrations in healthy individuals and in patients with diabetes mellitus, and the rate of Emptying is itself modulated by acute changes in glycaemia. Clinical implementation of incretin-based therapies for the management of T2DM, which diminish postprandial glycaemia, in part by slowing Gastric Emptying, is widespread. Other therapies for patients with T2DM, which specifically target Gastric Emptying include pramlintide and dietary-based treatment approaches. A weak association exists between upper gastrointestinal symptoms and the rate of Gastric Emptying. In patients with severe diabetic gastroparesis, pathological changes are highly variable and are characterized by loss of interstitial cells of Cajal and an immune infiltrate. Management options for patients with symptomatic gastroparesis remain limited in their efficacy, which probably reflects the heterogeneous nature of the underlying pathophysiology. The rate of Gastric Emptying is a critical determinant of postprandial glycaemia Disordered Gastric Emptying is common in patients with longstanding type 1 diabetes mellitus and type 2 diabetes mellitus; however, the prevalence and natural history of diabetic gastroparesis is poorly defined A number of management strategies for patients with type 2 diabetes mellitus specifically target Gastric Emptying A bidirectional relationship exists between the rate of Gastric Emptying and glycaemia, such that the rate of Gastric Emptying is partially modulated by acute changes in blood glucose concentrations In patients with severe diabetic gastroparesis, histological abnormalities are heterogeneous; however, presence of an immune infiltrate and loss of interstitial cells of Cajal are evident in the majority of patients Currently available management strategies for symptomatic diabetic gastroparesis have limited efficacy and further work in this area is required Disordered Gastric Emptying (also known as gastroparesis) is a complication frequently associated with long-standing type 1 diabetes mellitus and type 2 diabetes mellitus. In this Review, Phillips and colleagues discuss the underlying pathophysiology of gastroparesis in patients with diabetes mellitus. In addition, diagnosis, symptom management and emerging therapies are addressed.
-
Gastric Emptying and glycaemia in health and diabetes mellitus
Nature reviews. Endocrinology, 2014Co-Authors: Liza K. Phillips, Christopher K. Rayner, Karen L. Jones, Adam M. Deane, Michael HorowitzAbstract:The rate of Gastric Emptying is a critical determinant of postprandial glycaemia and, accordingly, is fundamental to maintaining blood glucose homeostasis. Disordered Gastric Emptying occurs frequently in patients with longstanding type 1 diabetes mellitus and type 2 diabetes mellitus (T2DM). A complex bidirectional relationship exists between Gastric Emptying and glycaemia--Gastric Emptying accounts for ∼35% of the variance in peak postprandial blood glucose concentrations in healthy individuals and in patients with diabetes mellitus, and the rate of Emptying is itself modulated by acute changes in glycaemia. Clinical implementation of incretin-based therapies for the management of T2DM, which diminish postprandial glycaemia, in part by slowing Gastric Emptying, is widespread. Other therapies for patients with T2DM, which specifically target Gastric Emptying include pramlintide and dietary-based treatment approaches. A weak association exists between upper gastrointestinal symptoms and the rate of Gastric Emptying. In patients with severe diabetic gastroparesis, pathological changes are highly variable and are characterized by loss of interstitial cells of Cajal and an immune infiltrate. Management options for patients with symptomatic gastroparesis remain limited in their efficacy, which probably reflects the heterogeneous nature of the underlying pathophysiology.
-
Measurement of Gastric Emptying in diabetes
Journal of diabetes and its complications, 2014Co-Authors: Liza K. Phillips, Christopher K. Rayner, Karen L. Jones, Michael HorowitzAbstract:Abstract There has been a substantial evolution of concepts related to disordered Gastric Emptying in diabetes. While the traditional focus has hitherto related to the pathophysiology and management of upper gastrointestinal symptoms associated with gastroparesis, it is now apparent that the rate of Gastric Emptying is central to the regulation of postprandial glycemia. This recognition has stimulated the development of dietary and pharmacologic approaches to optimize glycemic control, at least in part, by slowing Gastric Emptying. With the increased clinical interest in this area, it has proved necessary to expand the traditional indications for Gastric Emptying studies, and consider the relative strengths and limitations of available techniques. Scintigraphy remains the ‘gold standard’ for the measurement of Gastric Emptying, however, there is a lack of standardization of the technique, and the optimal test meal for the evaluation of gastrointestinal symptoms may be discordant from that which is optimal to assess impaired glycemic control. The stable isotope breath test provides an alternative to scintigraphy and can be performed in an office-based setting. The effect of glucagon-like peptide-1 (GLP-1) and its agonists to reduce postprandial glycemia is dependent on the baseline rate of Gastric Emptying, as well as the magnitude of slowing. Because the effect of exogenous GLP-1 to slow Gastric Emptying is subject to tachyphylaxis with sustained receptor exposure, ‘short acting’ or ‘prandial’ GLP-1 agonists primarily target postprandial glycemia through slowing of Gastric Emptying, while ‘long acting’ or ‘non-prandial’ agents lower fasting glucose primarily through insulinotropic and glucagonostatic mechanisms. Accordingly, the indications for the therapeutic use of these different agents are likely to vary according to baseline Gastric Emptying rate and glycemic profiles.
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Predictors of Delayed Gastric Emptying in Diabetes
Diabetes care, 2001Co-Authors: Karen L. Jones, Judith M. Wishart, Antonietta Russo, Julie E. Stevens, Melanie K. Berry, Michael HorowitzAbstract:OBJECTIVE —To define the predictors of the rate of Gastric Emptying in patients with diabetes. RESEARCH DESIGN AND METHODS —A total of 101 outpatients with diabetes (79 type 1 and 22 type 2) underwent measurements of Gastric Emptying of a solid/liquid meal (scintigraphy), upper gastrointestinal symptoms (questionnaire), glycemic control (blood glucose concentrations during Gastric Emptying measurement), and autonomic nerve function (cardiovascular reflexes). RESULTS —The Gastric Emptying of solid and/or liquid was delayed in 66 (65%) patients. Solid (retention at 100 min 64 ± 3.2 vs. 50.2 ± 3.6%, P P P CONCLUSIONS —We conclude that the presence of abdominal bloating/fullness but not any other upper gastrointestinal symptom is associated with diabetic gastroparesis and that Gastric Emptying is slower in diabetic women than in diabetic men.
Liza K. Phillips - One of the best experts on this subject based on the ideXlab platform.
-
Gastric Emptying and glycaemia in health and diabetes mellitus
Nature Reviews Endocrinology, 2015Co-Authors: Liza K. Phillips, Christopher K. Rayner, Karen L. Jones, Adam M. Deane, Michael HorowitzAbstract:The rate of Gastric Emptying is a critical determinant of postprandial glycaemia and, accordingly, is fundamental to maintaining blood glucose homeostasis. Disordered Gastric Emptying occurs frequently in patients with longstanding type 1 diabetes mellitus and type 2 diabetes mellitus (T2DM). A complex bidirectional relationship exists between Gastric Emptying and glycaemia—Gastric Emptying accounts for ∼35% of the variance in peak postprandial blood glucose concentrations in healthy individuals and in patients with diabetes mellitus, and the rate of Emptying is itself modulated by acute changes in glycaemia. Clinical implementation of incretin-based therapies for the management of T2DM, which diminish postprandial glycaemia, in part by slowing Gastric Emptying, is widespread. Other therapies for patients with T2DM, which specifically target Gastric Emptying include pramlintide and dietary-based treatment approaches. A weak association exists between upper gastrointestinal symptoms and the rate of Gastric Emptying. In patients with severe diabetic gastroparesis, pathological changes are highly variable and are characterized by loss of interstitial cells of Cajal and an immune infiltrate. Management options for patients with symptomatic gastroparesis remain limited in their efficacy, which probably reflects the heterogeneous nature of the underlying pathophysiology. The rate of Gastric Emptying is a critical determinant of postprandial glycaemia Disordered Gastric Emptying is common in patients with longstanding type 1 diabetes mellitus and type 2 diabetes mellitus; however, the prevalence and natural history of diabetic gastroparesis is poorly defined A number of management strategies for patients with type 2 diabetes mellitus specifically target Gastric Emptying A bidirectional relationship exists between the rate of Gastric Emptying and glycaemia, such that the rate of Gastric Emptying is partially modulated by acute changes in blood glucose concentrations In patients with severe diabetic gastroparesis, histological abnormalities are heterogeneous; however, presence of an immune infiltrate and loss of interstitial cells of Cajal are evident in the majority of patients Currently available management strategies for symptomatic diabetic gastroparesis have limited efficacy and further work in this area is required Disordered Gastric Emptying (also known as gastroparesis) is a complication frequently associated with long-standing type 1 diabetes mellitus and type 2 diabetes mellitus. In this Review, Phillips and colleagues discuss the underlying pathophysiology of gastroparesis in patients with diabetes mellitus. In addition, diagnosis, symptom management and emerging therapies are addressed.
-
Gastric Emptying and glycaemia in health and diabetes mellitus
Nature reviews. Endocrinology, 2014Co-Authors: Liza K. Phillips, Christopher K. Rayner, Karen L. Jones, Adam M. Deane, Michael HorowitzAbstract:The rate of Gastric Emptying is a critical determinant of postprandial glycaemia and, accordingly, is fundamental to maintaining blood glucose homeostasis. Disordered Gastric Emptying occurs frequently in patients with longstanding type 1 diabetes mellitus and type 2 diabetes mellitus (T2DM). A complex bidirectional relationship exists between Gastric Emptying and glycaemia--Gastric Emptying accounts for ∼35% of the variance in peak postprandial blood glucose concentrations in healthy individuals and in patients with diabetes mellitus, and the rate of Emptying is itself modulated by acute changes in glycaemia. Clinical implementation of incretin-based therapies for the management of T2DM, which diminish postprandial glycaemia, in part by slowing Gastric Emptying, is widespread. Other therapies for patients with T2DM, which specifically target Gastric Emptying include pramlintide and dietary-based treatment approaches. A weak association exists between upper gastrointestinal symptoms and the rate of Gastric Emptying. In patients with severe diabetic gastroparesis, pathological changes are highly variable and are characterized by loss of interstitial cells of Cajal and an immune infiltrate. Management options for patients with symptomatic gastroparesis remain limited in their efficacy, which probably reflects the heterogeneous nature of the underlying pathophysiology.
-
Measurement of Gastric Emptying in diabetes
Journal of diabetes and its complications, 2014Co-Authors: Liza K. Phillips, Christopher K. Rayner, Karen L. Jones, Michael HorowitzAbstract:Abstract There has been a substantial evolution of concepts related to disordered Gastric Emptying in diabetes. While the traditional focus has hitherto related to the pathophysiology and management of upper gastrointestinal symptoms associated with gastroparesis, it is now apparent that the rate of Gastric Emptying is central to the regulation of postprandial glycemia. This recognition has stimulated the development of dietary and pharmacologic approaches to optimize glycemic control, at least in part, by slowing Gastric Emptying. With the increased clinical interest in this area, it has proved necessary to expand the traditional indications for Gastric Emptying studies, and consider the relative strengths and limitations of available techniques. Scintigraphy remains the ‘gold standard’ for the measurement of Gastric Emptying, however, there is a lack of standardization of the technique, and the optimal test meal for the evaluation of gastrointestinal symptoms may be discordant from that which is optimal to assess impaired glycemic control. The stable isotope breath test provides an alternative to scintigraphy and can be performed in an office-based setting. The effect of glucagon-like peptide-1 (GLP-1) and its agonists to reduce postprandial glycemia is dependent on the baseline rate of Gastric Emptying, as well as the magnitude of slowing. Because the effect of exogenous GLP-1 to slow Gastric Emptying is subject to tachyphylaxis with sustained receptor exposure, ‘short acting’ or ‘prandial’ GLP-1 agonists primarily target postprandial glycemia through slowing of Gastric Emptying, while ‘long acting’ or ‘non-prandial’ agents lower fasting glucose primarily through insulinotropic and glucagonostatic mechanisms. Accordingly, the indications for the therapeutic use of these different agents are likely to vary according to baseline Gastric Emptying rate and glycemic profiles.
