Mediation of hyperglycemia-evoked gastric slow-wave dysrhythmias by endogenous prostaglandins

Hasler, William L.; Soudah, Hani C.; Dulai, Gareth S.; Owyang, Chung

doi:10.1016/0016-5085(95)90445-x

Cited by 206 publications

(155 citation statements)

References 23 publications

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“…Gastric emptying of solids consists of two phases: the lag phase, corresponding to meal transportation from the fundus to the antrum (20), and the postlag phase, corresponding to the propulsion of solid food particles through the pylorus (20). Hyperglycemia slows gastric emptying of solids by prolonging the lag phase and decreasing the postlag emptying rate (14) via reduced proximal gastric tone (21), suppression of antral pressure waves (22), and stimulation of pyloric contractions (23). The magnitude of deceleration of emptying, the prolongation of the lag phase, and the slowing of the postlag emptying rate that we observed during hyperglycemia are consistent with these previous studies (20,22,23).…”

Section: Discussionmentioning

confidence: 99%

“…Hyperglycemia slows gastric emptying of solids by prolonging the lag phase and decreasing the postlag emptying rate (14) via reduced proximal gastric tone (21), suppression of antral pressure waves (22), and stimulation of pyloric contractions (23). The magnitude of deceleration of emptying, the prolongation of the lag phase, and the slowing of the postlag emptying rate that we observed during hyperglycemia are consistent with these previous studies (20,22,23). Purported mechanisms governing this response include nitrergic pathways (24), direct stimulation of glucose-dependent neurons within the myenteric plexus (25), and suppression of vagal cholinergic activity, which has been demonstrated via reduced pancreatic polypeptide levels during hyperglycemia (26).…”

Section: Discussionmentioning

confidence: 99%

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Hyperglycemia Potentiates the Slowing of Gastric Emptying Induced by Exogenous GLP-1

et al. 2015

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OBJECTIVEAcute hyperglycemia markedly slows gastric emptying. Exogenous GLP-1 also slows gastric emptying, leading to diminished glycemic excursions. The primary objective was to determine whether hyperglycemia potentiates the slowing of gastric emptying induced by GLP-1 administration. RESEARCH DESIGN AND METHODSTen healthy participants were studied on 4 separate days. Blood glucose was clamped at hyperglycemia using an intravenous infusion of 25% dextrose (∼12 mmol/L; hyper) on 2 days, or maintained at euglycemia (∼6 mmol/L; eu) on 2 days, between t = 215 and 240 min. During hyperglycemic and euglycemic days, participants received intravenous GLP-1 (1.2 pmol/kg/min) and placebo in a randomized double-blind fashion. At t = 0 min, subjects ingested 100 g beef mince labeled with 20 MBq technetium-99m-sulfur colloid and 3 g 3-O-methyl-glucose (3-OMG), a marker of glucose absorption. Gastric emptying was measured scintigraphically from t = 0 to 240 min and serum 3-OMG taken at regular intervals from t = 15 to 240 min. The areas under the curve for gastric emptying and 3-OMG were analyzed using one-way repeated-measures ANOVA with Bonferroni-Holm adjusted post hoc tests. RESULTSHyperglycemia slowed gastric emptying (eu/placebo vs. hyper/placebo; P < 0.001) as did GLP-1 (eu/placebo vs. eu/GLP-1; P < 0.001). There was an additive effect of GLP-1 and hyperglycemia, such that gastric emptying was markedly slower compared with GLP-1 administration during euglycemia (eu/GLP-1 vs. hyper/GLP-1; P < 0.01). CONCLUSIONSAcute administration of exogenous GLP-1 profoundly slows gastric emptying during hyperglycemia in excess of the slowing induced by GLP-1 during euglycemia. Studies are required to determine the effects of hyperglycemia on gastric emptying with the subcutaneously administered commercially available GLP-1 agonists in patients with type 2 diabetes.Gastric emptying is a major determinant of postprandial glycemia in health, as well as in type 1 and type 2 diabetes (1,2), and accounts for ;35% of the variance in the initial glycemic response to oral carbohydrate (1). Accordingly, dietary and pharmacological strategies that slow gastric emptying, including short-acting GLP-1 agonists, are useful interventions to attenuate postprandial glycemic excursions and overall glycemia in type 2 diabetes (3).

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Hyperglycemia Potentiates the Slowing of Gastric Emptying Induced by Exogenous GLP-1

et al. 2015

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“…Acute hyperglycaemia has been shown to induce relaxation of the proximal stomach, suppression of the frequency and propagation of antral pressure waves, and an increase in pyloric tone. Moreover, marked hyperglycaemia can also produce tachygastria and un-coordinated motor activity of different parts of the stomach [8,9]. Studies have also shown that acute hyperglycaemia slows gastric emptying of both solid and liquid nutrients in patients with established autonomic neuropathy and can also attenuate the prokinetic effect of intravenous erythromycin on gastric emptying [5,10].…”

Section: Discussionmentioning

confidence: 99%

The role of continuous subcutaneous insulin infusion therapy in patients with diabetic gastroparesis

et al. 2011

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Aims/objective To describe the effectiveness of continuous subcutaneous insulin infusion (CSII) in patients with symptomatic diabetic gastroparesis and unstable glycaemic control. Methods Data from 26 patients with symptomatic diabetic gastroparesis and unstable glycaemic control using multiple-dose insulin (MDI) regimens, and subsequently managed with CSII, were analysed. Results Following initiation of CSII, the median length of inpatient bed days associated with hospital admissions related to gastroparesis and glycaemic instability was reduced from 8.5 (range 0-144) days patient −1 year −1 prior to CSII to 0 (range 0-15) days patient −1 year −1 .The median HbA 1c reduction with CSII was 1.8% (22 mmol/mol; p<0.05). The median capillary blood glucose (CBG) with CSII was significantly lower than with MDI: 7.7 mmol/l (range 3.8-15.4 mmol/l) vs 9.8 mmol/l (range 2.3-27 mmol/l), respectively, p<0.001. Glycaemic variability with CSII was significantly reduced compared with MDI: CBG CV 0.37 vs CV 0.53, respectively, p<0.001. Conclusions/interpretation CSII therapy in patients with diabetic gastroparesis results in significant improvement in glycaemic control and reductions in glycaemic variability and number of hospital inpatient bed days.

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“…Relatos de que prostaglandinas estão envolvidas na mediação do ritmo elétrico gástrico anormal durante hiperglicemia e de que administração de indometacina pode prevenir taquigastria em indivíduos saudáveis 36 indicam a provável natureza inflamatória das alterações motoras do TGI associadas ao DM em geral. Tal achado é reforçado por outras pesquisas que demonstraram inflamação associada à degeneração neurológica, que pode levar a alterações secundárias de motilidade 37 .…”

Section: Figura 1 -Mecanismos Fisiopatogênicos Dos Sintomas Gastrointunclassified

Mechanisms and factors associated with gastrointestinal symptoms in patients with diabetes mellitus

Rodrigues

Motta

2012

J Pediatr (Rio J)

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Objectives: To present the main mechanisms that cause gastrointestinal symptoms in patients with diabetes mellitus, their frequency, and controversies as to their occurrence in children and adolescents.Sources: Non-systematic review of the literature conducted in the MEDLINE/PubMed and SciELO databases , as well as relevant book chapters. The most relevant and up-to-date articles on the topic were selected. Summary of the findings:Prevalence of diabetes mellitus has been increasing over the years in many countries. The complications caused by this disease in the digestive system, such as gastrointestinal symptoms (nausea, vomiting, abdominal pain, heartburn, dysphagia, constipation, diarrhea, and fecal incontinence) are well known. The pathogenesis of changes in the gastrointestinal functions in patients with diabetes mellitus is still being investigated at the same time as the role of the enteric nervous system and its neurotransmitters has gained significance. As a consequence of the complications in the digestive system, which damage the enteric nervous system, patients with diabetes mellitus may have specific gastrointestinal motility disorders, some of which may be of great relevance, such as diabetic gastroparesis, constipation, and diarrhea. Gastrointestinal dysfunction increases the morbidity of diabetes mellitus and worsens the quality of life of diabetic individuals. Conclusions:There are few studies addressing these problems in childhood and adolescence. Diabetes mellitus affects the digestive system over the years. Because this condition worsens the quality of life of diabetic individuals and leads to complications, attention must be paid to gastrointestinal symptoms when treating patients with diabetes mellitus. J Pediatr (Rio J). 2012;88(1):17-24:Diabetes mellitus, digestive signs and symptoms, gastrointestinal motility, etiology, child, adolescent. ResumoObjetivos: Apresentar a frequência, os principais fatores causadores dos sintomas gastrointestinais em pacientes portadores do diabetes melito e controvérsias quanto à sua ocorrência em crianças e adolescentes. Fontes dos dados:Revisão não sistemática nas bases de dados MEDLINE/PubMed e SciELO (1983-2011), além de capítulos de livros relevantes. Foram selecionados os artigos mais atuais e representativos do tema. Síntese dos dados:A prevalência do diabetes melito vem aumentando ao longo dos anos em vários países do mundo. No sistema digestório, é conhecida a ocorrência de complicações do diabetes melito, entre elas os sintomas gastrointestinais (náuseas, vômitos, dor abdominal, azia, disfagia, constipação, diarreia e incontinência fecal). A patogênese das alterações das funções gastrointestinais no diabetes melito está ainda sob investigação, e o papel do sistema nervoso entérico e seus neurotransmissores tem ganhado significância. Em decorrência do comprometimento do sistema digestório, com danos ao sistema nervoso entérico, portadores do diabetes melito podem apresentar quadros específicos de distúrbios de motilidade, alguns de grande re...

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Mediation of hyperglycemia-evoked gastric slow-wave dysrhythmias by endogenous prostaglandins

Cited by 206 publications

References 23 publications

Hyperglycemia Potentiates the Slowing of Gastric Emptying Induced by Exogenous GLP-1

Hyperglycemia Potentiates the Slowing of Gastric Emptying Induced by Exogenous GLP-1

The role of continuous subcutaneous insulin infusion therapy in patients with diabetic gastroparesis

Mechanisms and factors associated with gastrointestinal symptoms in patients with diabetes mellitus

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