Implication of neurohormonal-coupled mechanisms of gastric emptying and pancreatic secretory function in diabetic gastroparesis

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Term Occurence Count Dictionary
Insulin 1 endocrinologydiseasesdrugs
diabetes mellitus 1 endocrinologydiseases
hyperglycemia 5 endocrinologydiseases
hypoglycemia 8 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Insulin 41884 This due to several factors including delayed gastric emptying and subsequent slow absorption of food. Insulin is an important therapeutic agent mainly for patients with type 1 DM however, type 2 DM patients also
Select Disease Character Offset Disease Term Instance
diabetes mellitus 3821 solids by scintigraphy[[6]].Given the fact that more than 30% of gastroparesis cases are related to diabetes mellitus (DM), several studies have investigated the pathophysiological nature of diabetic gastroparesis (DGP)[[7]].
hyperglycemia 28068 The unique and powerful stimulatory effects of GLP-1 on insulin secretion in response to postprandial hyperglycemia have well documented using GLP-1 receptor agonists and antagonists. Interestingly, the application of
hyperglycemia 30759 mechanisms are well maintained in healthy subjects and therefore any increase in digested glucose ( hyperglycemia ) stimulates insulin secretion and reduces glucagon levels. Similarly, feedback mechanisms are initiated
hyperglycemia 31089 which under normal physiological conditions, increases gastric emptying. However, during postprandial hyperglycemia , the secretion of this hormone is suppressed so that the gastric emptying is inhibited[[102]].Figure
hyperglycemia 31599 physiological conditions that control postprandial glycemia, it is not surprising to know that pronounced hyperglycemia in both Type 1 DM and Type 2 DM is associated with several abnormalities in gastric motility including
hyperglycemia 31971 challenged by the fact that patients with Type 1 DM also experienced delayed gastric emptying in response to hyperglycemia [[105],[106]]. On the other hand, it was found that insulin-induced hypoglycemia was sufficient to provoke
hypoglycemia 5410 studies have demonstrated that patients with DGP experience a blunted postprandial glucose response and hypoglycemia which further complicates the management of DM in this group of patients. These findings highlight an
hypoglycemia 32052 emptying in response to hyperglycemia[[105],[106]]. On the other hand, it was found that insulin-induced hypoglycemia was sufficient to provoke a counter-regulatory mechanism which involves acceleration of gastric emptying[[107]].One
hypoglycemia 40484 associated with chronic pancreatitis is due to dysfunction of autonomic nerves.Impaired awareness of hypoglycemia is another important aspect that highlights the interrelationship between the neurohormonal components
hypoglycemia 40671 the neurohormonal components and the postprandial glycemic control.Previous research has shown that hypoglycemia is not only associated with transient impairment of cognition but also with high rates of functional
hypoglycemia 40899 morbidity[[142]]. It is well documented that type 1 DM patients experience at least two episodes of hypoglycemia per week and this represents a significant challenge in the clinical practice to achieve optimal therapeutic
hypoglycemia 41088 practice to achieve optimal therapeutic targets that involves insulin regimens[[143]].A normal response to hypoglycemia includes an activation of a complex and sensitive counter-regulatory response leads eventually to a
hypoglycemia 41753 DM[[144]].Interestingly, recent studies have demonstrated that diabetic patients with DGP experience episodes hypoglycemia more frequent. This due to several factors including delayed gastric emptying and subsequent slow absorption
hypoglycemia 42243 gastric emptying and slow absorption of food. This, in turn, leads to frequent episodes of postprandial hypoglycemia .CONCLUSIONThe dramatic increase in the prevalence of DGP has directed significant attention to the pathophysiology

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