Studies on the Viability of the Isolated Vascularly Perfused Rat Colon

Herrmann-Rinke, C.; Eissele, Rolf; Arnold, R.; Göke, Burkhard

doi:10.1159/000201356

Cited by 10 publications

(5 citation statements)

References 19 publications

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“…Both glucosidase inhibitors clearly had the ability to enhance the release of GLP-1 from the lower intestine significantly. That the L cells of the lower intestine are capable of releasing the gut peptide upon luminal stimulation has also been demonstrated by in vitro experiments with isolated bowel segments [18].…”

Section: Discussionmentioning

confidence: 76%

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GLP-1 Release in Man after Lower Large Bowel Resection or Intrarectal Glucose Administration

Printz¹,

Reiter²,

Samadi³

et al. 1998

Digestion

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Background: This study addresses the question whether the insulinotropic gut hormone, glucagon-like peptide-1 (GLP-1), is released from the lower large bowel upon oral or rectal glucose uptake. Methods: It was evaluated whether rectum or sigmoid colon resection alters glucose homeostasis or the plasma levels of the insulinotropic gut hormone, gastric inhibitory polypeptide (GIP), or GLP-1. Six men and 3 women (age 63 ± 8 years, BMI 25.4 ± 4.0 kg/m²) with normal preoperative fasting glucose values were treated before and after resection of large bowel segments. Fasting oral glucose tolerance (OGT, 75 g glucose/300 ml) tests were performed both before and 10 days postoperatively. Another approach aimed to clarify whether luminal glucose stimulation in the rectum/sigmoid colon increases GLP-1 plasma levels. Ten healthy volunteers (4 males, 6 females, age 25 ± 2 years, BMI 22.1 ± 2.4 kg/m²) received enemas with both saline and, 7 days later, 1 g/kg body weight glucose (70% glucose solution) intrarectally. Results: Neither rectum nor sigmoid colon resection led to significant changes in the pre- and postoperative glucose responses to OGT testing, or insulin, GIP and GLP-1 release. Intrarectal glucose instillation increased blood glucose by about 10 mg/dl with parallel small elevations in immunoreactive insulin and immunoreactive C peptide. However, plasma GLP-1 levels remained unaltered. Conclusion: Our data make it unlikely that GLP-1 derived from the lower large bowel contributes significantly to maintain normal glucose tolerance.

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Section: Discussionmentioning

confidence: 76%

“…In the in vitro system, glucose was able to enhance GLP-1 secretion in the venous effluent [18]. In the in vivo situation, instillation of glucose into the distal large bowel was not able to enhance GLP-1 to a significant extent in plasma, although the human rectum contains the largest amount of GLP-1-producing L cells [5].…”

Section: Discussionmentioning

confidence: 88%

GLP-1 Release in Man after Lower Large Bowel Resection or Intrarectal Glucose Administration

Printz¹,

Reiter²,

Samadi³

et al. 1998

Digestion

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“…The model of an isolated, vascularly perfused rat colon has been described in detail elsewhere [21,22]. Each colon preparation was used just for one perfusion trial.…”

Section: Preparation Of the Isolated Perfused Rat Colonmentioning

confidence: 99%

Effect of Naloxone-3-Glucuronide and N-Methylnaloxone on the Motility of the Isolated Rat Colon After Morphine

et al. 2007

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The effect of the opioid antagonists naloxone-3-glucuronide and N-methylnaloxone on rat colon motility after morphine stimulation was measured. The rat model consisted of the isolated, vascularly perfused colon. The antagonists (10(-4) M, intraluminally) and morphine (10(-4) M, intra-arterially) were administered from 20 to 30 and from 10 to 50 min, respectively. Colon motility was determined by the luminal outflow. The antagonist concentrations in the luminal and venous outflow were measured by high-performance liquid chromatography. Naloxone-3-glucuronide and N-methylnaloxone reversed the morphine-induced reduction of the luminal outflow to baseline within 10 and 20 min, respectively. These antagonists were then excreted in the luminal outflow and could not be found in the venous samples. Naloxone, produced by hydrolysis or demethylation, was not detectable. In conclusion, highly polar naloxone derivatives peripherally antagonize the motility-lowering effect of morphine in the perfused isolated rat colon, are stable, and are not able to cross the colon-mucosal blood barrier.

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“…It has been shown that the vagal nerve mediates the early response of L cells to nutrients in rats (21). Among the different neuromediators previously tested for their capacity to stimulate GLP-1 release, carbachol, a cholinergic agonist, and GRP were shown to stimulate GLP-1 release in cellular and organ models (7,8,22). NCI-H716 cells incubated during 2 h with increasing concentrations of carbachol showed a dose-dependent increase in GLP-1 release, with a maximum of 1.5 Ϯ 0.2-fold at the maximal dose tested (1 mm; Fig.…”

Section: The Neuromediator Gastrin-releasing Peptide (Grp) and The Chmentioning

confidence: 99%

A Human Cellular Model for Studying the Regulation of Glucagon-Like Peptide-1 Secretion

et al. 2001

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GLP-1 (glucagon-like peptide-1) is a potent insulin secretagogue released from L cells in the intestine. The regulation of GLP-1 secretion has been described both in vivo and in vitro in several animal species, but data from human cellular models are lacking. For this purpose, factors and cell-signaling pathways regulating GLP-1 secretion were investigated in the NCI-H716 human intestinal cell line. After differentiation, these cells homogeneously produced 16.8 pmol GLP-1/mg protein with a basal release of 4.2% during a 2-h incubation period. Nutrients, such as palmitic acid, oleic acid, and meat hydrolysate, stimulated GLP-1 secretion in a dose-dependent manner, as did the cholinergic agonist carbachol and the neuromediator gastrin-releasing peptide. Along with stimulating GLP-1 release, gastrin-releasing peptide, like ionomycin, increased intracellular calcium levels. Activators of PKA and PKC were able to increase GLP-1 secretion in NCI-H716 cells. However, neither PKA activators nor meat hydrolysate increased proglucagon mRNA levels. These findings indicate that the NCI-H716 cell line constitutes a unique model to study the cellular mechanism of GLP-1 secretion in humans and suggest potential interspecies divergence in the regulation of proglucagon gene expression in enteroendocrine cells.

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Studies on the Viability of the Isolated Vascularly Perfused Rat Colon

Cited by 10 publications

References 19 publications

GLP-1 Release in Man after Lower Large Bowel Resection or Intrarectal Glucose Administration

GLP-1 Release in Man after Lower Large Bowel Resection or Intrarectal Glucose Administration

Effect of Naloxone-3-Glucuronide and N-Methylnaloxone on the Motility of the Isolated Rat Colon After Morphine

A Human Cellular Model for Studying the Regulation of Glucagon-Like Peptide-1 Secretion

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