Release of glucagon-like peptide-1 (GLP-1) by carbohydrates in the perfused rat ileum

Ritzel, Uwe; Fromme, Albert; Ottleben, M; Leonhardt, U.; Ramadori, Giuliano

doi:10.1007/s005920050059

Cited by 90 publications

(73 citation statements)

References 15 publications

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“…The idea that low concentrations of glucose trigger GLP-1 release through metabolism and K ATP channel closure seems contrary to results obtained using perfused rat ileum, which showed that some nonmetabolizable glucose analogues also stimulate GLP-1 release (35). The ileal perfusion experiments, however, tested substrates at much higher concentrations (ϳ250 mmol/l) than those used in the current study, and might stimulate secretion by an alternative mechanism.…”

Section: Discussioncontrasting

confidence: 91%

Glucose-Sensing in Glucagon-Like Peptide-1-Secreting Cells

Reimann

Gribble²

2002

Diabetes

257

231

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Section: Discussioncontrasting

confidence: 91%

Glucose-Sensing in Glucagon-Like Peptide-1-Secreting Cells

Reimann

Gribble²

2002

Diabetes

257

231

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“…It should also be noted that major differences between species are evident with regards to incretin hormone release. For example, fructose stimulates the release of GLP-1 in rats (38) and humans (36) but not in dogs (41).…”

Section: Discussionmentioning

confidence: 99%

Effect of the artificial sweetener, sucralose, on gastric emptying and incretin hormone release in healthy subjects

Bellon

Wishart

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

218

160

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“…Earlier studies examining the sugar specificity of gut peptide responses in the intact intestine concluded that sugar absorption was important for hormone stimulation. Glucose-triggered secretion exhibited a requirement for luminal Na + ions and was mimicked by metabolisable as well as non-metabolisable substrates of the brush border monosaccharide transporter system (40)(41)(42) . The results indicated that glucose uptake rather than metabolism was critical for GLP-1 and GIP secretion.…”

Section: Carbohydrate Sensingmentioning

confidence: 99%

“…Consistent with this idea, intestinal GLP-1 content and secretion were found to be impaired in GLUT2 knockout mice (48) . The observed small GLP-1 response to oral fructose might also be attributable to metabolism (41) , as apical fructose uptake is mediated by GLUT5, whose activity does not generate an electrical signal.…”

Section: Carbohydrate Sensingmentioning

confidence: 99%

The gut endocrine system as a coordinator of postprandial nutrient homoeostasis

Gribble¹

2012

Proc. Nutr. Soc.

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Hormones from the gastrointestinal (GI) tract are released following food ingestion and trigger a range of physiological responses including the coordination of appetite and glucose homoeostasis. The aim of this review is to discuss the pathways by which food ingestion triggers secretion of cholecystokinin (CCK), glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) and the altered patterns of gut hormone release observed following gastric bypass surgery. Our understanding of how ingested nutrients trigger secretion of these gut hormones has increased dramatically, as a result of physiological studies in human subjects and animal models and in vitro studies on cell lines and primary intestinal cultures. Specialised enteroendocrine cells located within the gut epithelium are capable of directly detecting a range of nutrient stimuli through a range of receptors and transporters. It is concluded that the arrival of nutrients at the apical surface of enteroendocrine cells is a major stimulus for gut hormone release, thereby coupling these endocrine signals to the arrival of absorbed nutrients in the bloodstream.Glucagon-like peptide-1: Cholecystokinin: Glucose-dependent insulinotropic polypeptide:Enteroendocrine: Diabetes: Obesity Physiological responses to food ingestion include the regulation of appetite and glucose homoeostasis as well as the control of gastric motility and secretion. Although rising circulating nutrient concentrations act as a sign of recent food intake, however, they do not indicate whether the nutrients are of alimentary origin and therefore do not convey sufficient information to enable the body to handle them appropriately. This role is fulfilled by neurohormonal signals from the gut, which indicate the volume and content of ingested food. A number of enteric peptides have been implicated in signalling from the gut to the brain and the pancreas. These include cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and peptide YY (PYY), which target receptors in the pancreas and enteric and central nervous systems. Interest in gut peptides has increased in recent decades, with the finding that they have profound and sustained physiological effects on appetite and insulin release (1)(2)(3)(4) . GLP-1, an incretin hormone that stimulates insulin release and reduces food intake, has been very successfully exploited for the treatment of type-2 diabetes. Injectable GLP-1 mimetics and orally available inhibitors of GLP-1 degradation (DPP4 inhibitors) are now widely prescribed and match the effectiveness of other oral therapies on glycaemic control, but are additionally weight-lowering, or at least weight-neutral, and are associated with a low incidence of hypoglycaemic side effects (5) . Recent excitement in the gut peptide field has been triggered by the results of using gastric bypass surgery as a treatment for morbid obesity. Somewhat unexpectedly, it was observed that a number of bariatric procedures have effec...

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Release of glucagon-like peptide-1 (GLP-1) by carbohydrates in the perfused rat ileum

Cited by 90 publications

References 15 publications

Glucose-Sensing in Glucagon-Like Peptide-1-Secreting Cells

Glucose-Sensing in Glucagon-Like Peptide-1-Secreting Cells

Effect of the artificial sweetener, sucralose, on gastric emptying and incretin hormone release in healthy subjects

The gut endocrine system as a coordinator of postprandial nutrient homoeostasis

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