Somatostatin receptor 5 and cannabinoid receptor 1 activation inhibit secretion of glucose-dependent insulinotropic polypeptide from intestinal K cells in rodents

Moss, Catherine E.; Marsh, W.; Parker, Helen; Ogunnowo-Bada, Emmanuel; Riches, Christine H.; Habib, Abdella M.; Evans, Mark L.; Gribble, Fiona M.; Reimann, Frank

doi:10.1007/s00125-012-2663-5

Cited by 69 publications

(61 citation statements)

References 36 publications

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“…Five somatostatin receptors (SSTRs) have been identified, all thought to be G i -coupled, leading to inhibition of adenylyl cyclase and a reduction in intracellular cAMP levels. In GLUTag and primary L cells, somatostatin is believed to inhibit GLP1 and PYY release via SSTR5 (94). Ghrelin secretion is also inhibited by somatostatin, potentially involving SSTR1, -2, and -3 (48).…”

Section: Sensing Of Non-nutrient Stimulimentioning

confidence: 99%

Gut chemosensing mechanisms

Psichas¹,

Reimann²,

Gribble³

2015

J. Clin. Invest.

210

176

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Section: Sensing Of Non-nutrient Stimulimentioning

confidence: 99%

Gut chemosensing mechanisms

Psichas¹,

Reimann²,

Gribble³

2015

J. Clin. Invest.

210

176

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“…Octreotide suppressed not only plasma GLP-1 but also GIP concentration within 15 minutes during 75 g-OGTT. Somatostatin receptors exist as five isoforms (SSTR1-SSTR5), of which sst5 is expressed by the rat L-cell and the rodent K-cell [18,19]. Somatostatin inhibits GIP and GLP-1 secretion from small intestinal cultures through SSTR5 [17].…”

Section: Fig 2 Continuous Glucose Monitoring (Cgm) Over 24 Hoursmentioning

confidence: 99%

Octreotide improves early dumping syndrome potentially through incretins: a case report

et al. 2013

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Dumping synDrome, or rapid gastric emptying, is a serious complication that may occur after gastric surgery in approximately 5-10% of patients, although it may occur in approximately 20% after vagotomy with pyloroplasty and up to 50% after esophagectomy [1][2][3]. In spite of this level of occurrence, the pathophysiologic mechanisms underlying the symptoms of dumping syndrome are poorly understood. Here, we report a patient with dumping syndrome following distal gastrectomy with Billroth I reconstruction for early-stage gastric cancer. In this case, we have measured the levels of several hormones during a 75g oral glucose tolerance test (75g-OGTT), and found that glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) were both inhibited by octreotide treatment. Abstract. Dumping syndrome, or rapid gastric emptying, is a frequent complication after gastric surgery. In this case, the patient was a 47-year-old woman who 10 years previously had undergone distal gastrectomy with Billroth I reconstruction for early-stage gastric cancer. She presented with symptoms of weakness, headache, palpitation, sweating, dizziness and significant fatigue between one and two hours after a meal. Because a 75g oral glucose tolerance test (75g-OGTT) induced both acute postprandial tachycardia (within 1 hour) and postprandial hypoglycemia, we diagnosed this patient with early and late dumping syndrome. Dietary measures and acarbose improved symptoms of late dumping syndrome but did not prevent the symptoms of early dumping syndrome such as postprandial tachycardia, weakness, headache, palpitation, and dizziness. We therefore used the somatostatin analogue octreotide, which has been reported as an effective therapy for early dumping syndrome. Octreotide prevented the symptoms of early dumping syndrome, especially postprandial tachycardia, but caused postprandial hyperglycemia. Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) were completely suppressed during the 75g-OGTT following subcutaneous injection of octreotide. No change was observed in vasoactive intestinal polypeptide (VIP), which is the gastrointestinal peptide hormone generally responsible for early dumping syndrome, suggesting possible contribution of incretins in early dumping syndrome of this patient.Key words: Dumping syndrome, GLP-1, Octreotide material and methods Laboratory analysesBlood samples were taken after an overnight fast. Plasma glucose concentrations were measured with the hexokinase G6PD UV method. Serum insulin concentrations were measured with a chemiluminescent enzyme immunoassay. Serum triglyceride concentrations were determined by Enzymatic method. Serum total cholesterol concentrations were measured by a cholesterol dehydrogenase ultraviolet method. Serum HDL cholesterol concentrations were determined by a direct method (Cholestest ® N HDL, Sekisui Medical, Japan). Hemoglobin A1c (NGSP) levels were measured by high performance liquid chromatographic assay (HPLC). Serum total GIP and...

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“…Previous studies employing several experimental models including single K-and L-cells have shown that the hormones are secreted in response, for example, to glucose, which after entry via the sodium-glucose transporter-1 results in membrane depolarization and exocytosis secondary to calcium influx in both cell types (Reimann et al 2008, Parker et al 2009. Other studies have shown that stimuli activating the cAMP system may also result in both GLP1 and GIP secretion (Simpson et al 2007, Moss et al 2012, Hauge et al 2014, Svendsen et al 2015.…”

Section: Introductionmentioning

confidence: 99%

GLP1- and GIP-producing cells rarely overlap and differ by bombesin receptor-2 expression and responsiveness

Svendsen¹,

Pais²,

Engelstoft³

et al. 2015

Journal of Endocrinology

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The incretin hormones glucagon-like peptide-1 (GLP1) and glucose-dependent insulinotropic polypeptide (GIP) are secreted from intestinal endocrine cells, the so-called L-and K-cells. The cells are derived from a common precursor and are highly related, and co-expression of the two hormones in so-called L/K-cells has been reported. To investigate the relationship between the GLP1-and GIP-producing cells more closely, we generated a transgenic mouse model expressing a fluorescent marker in GIP-positive cells. In combination with a mouse strain with fluorescent GLP1 cells, we were able to estimate the overlap between the two cell types. Furthermore, we used primary cultured intestinal cells and isolated perfused mouse intestine to measure the secretion of GIP and GLP1 in response to different stimuli. Overlapping GLP1 and GIP cells were rare (w5%). KCl, glucose and forskolinCIBMX increased the secretion of both GLP1 and GIP, whereas bombesin/ neuromedin C only stimulated GLP1 secretion. Expression analysis showed high expression of the bombesin 2 receptor in GLP1 positive cells, but no expression in GIP-positive cells. These data indicate both expressional and functional differences between the GLP1-producing 'L-cell' and the GIP-producing 'K-cell'.

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Somatostatin receptor 5 and cannabinoid receptor 1 activation inhibit secretion of glucose-dependent insulinotropic polypeptide from intestinal K cells in rodents

Cited by 69 publications

References 36 publications

Gut chemosensing mechanisms

Gut chemosensing mechanisms

Octreotide improves early dumping syndrome potentially through incretins: a case report

GLP1- and GIP-producing cells rarely overlap and differ by bombesin receptor-2 expression and responsiveness

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