Effects of four orally administered analogues of prostaglandin E<sub>1</sub> and E<sub>2</sub> on glucose tolerance and on the secretion of pancreatic and gastrointestinal hormones in man

Nauck, Michael A.; Harter, Scott; Ebert, R.; Creutzfeldt, W.

doi:10.1111/j.1365-2362.1989.tb00233.x

Cited by 8 publications

(3 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…While some reports describe an inhibition of insulin and GIP [37], others have found the converse [38] or no change in insulin, but a decrease in GIP [39]. Decreased GIP levels have recently been reported after misoprostol administration to human volunteers [40], No significant effects on insulin or GIP were ob served in the present study.…”

Section: Discussioncontrasting

confidence: 49%

Plasma and Tissue Hormones in the Dog after Administration of the Prostaglandin Analogue, Misoprostol

Goodlad

Ghatei²,

Bloom³

et al. 1992

Digestion

View full text Add to dashboard Cite

Dogs were given a prostaglandin analogue, misoprostol, at a dose that significantly increases gastrointestinal epithelial cell proliferation. Both basal and postprandial concentrations of gastrin were significantly higher in the misoprostol-treated dogs and more than doubled after the meal in both the controls and in the test group. Plasma enteroglucagon, cholecystokinin, insulin and glucose-dependent insulinotrophic peptide all increased postprandially, with no effect of misoprostol. Tissue concentrations of bombesin, gastrin and somatostatin were unaffected by misoprostol, but the fundic gmcagon-like immunoreactivity was significantly increased. Thus high doses of misoprostol have only minor effects on gastrointestinal regulatory peptides, suggesting that the trophic effect of prostaglandins on the intestinal tract may be direct.

show abstract

Section: Discussioncontrasting

confidence: 49%

Plasma and Tissue Hormones in the Dog after Administration of the Prostaglandin Analogue, Misoprostol

Goodlad

Ghatei²,

Bloom³

et al. 1992

Digestion

View full text Add to dashboard Cite

show abstract

“…In vivo and in vitro immunoneutralization studies using antisera against different epitomes of GIP abolished only 20% to 50% of the incretin effect. 37,38 Further, it has been shown that the abolition of insulin release caused by an oral glucose load leaves the incretin effect nearly untouched, 39 raising even more doubt that GIP has an exclusive role in the enteroinsular axis. We found that motilin also stimulated the endogenous release of insulin in duodenectomized dogs.…”

Section: Discussionmentioning

confidence: 99%

Effect of Duodenectomy on Gastric Motility and Gastric Hormones in Dogs

Suzuki¹,

Mochiki²,

Haga³

et al. 2001

Annals of Surgery

View full text Add to dashboard Cite

ObjectiveTo test the hypothesis that the duodenum is required to coordinate interdigestive insulin secretion with gastrointestinal motility and to determine whether duodenectomy alters the interdigestive cycles of plasma motilin and insulin levels and their relations to insulin secretion and motility. MethodsAdult mongrel dogs were chronically implanted with force transducers in the stomach, duodenum, and upper jejunum to monitor contractile activity. Eight healthy mongrel dogs were divided into control and duodenectomized dogs. Insulin secretion, gastrointestinal motility, and plasma concentrations of motilin during the interdigestive period were measured in normal and duodenectomized dogs. ResultsAfter duodenectomy, no obvious phase III contractions were seen in the gastric antrum, but migrating phase III contractions were seen in the upper jejunum. The plasma motilin concentration did not fluctuate as it does in normal dogs, and remained low. After duodenectomy, insulin secretory cycles were not coordinated with either cycles of interdigestive motility or the plasma concentration of motilin. Exogenous motilin administration stimulated endogenous insulin release significantly compared with saline-treated controls. The contractile response of the stomach to exogenous motilin after duodenectomy was similar to that of intact dogs. ConclusionsDuodenectomy disrupts the relation between cycles of both interdigestive gastrointestinal motility and insulin secretion. These effects of duodenectomy may be attributable to interruption of the duodenopancreatic neural connections, hormonal abnormalities, or loss of vagus-sensitive humoral factors. The duodenum, which stores motilin, seems to play an important role in the relations between gastric migrating motor complexes and the concomitant increase of insulin secretion in fasted dogs. The mechanism responsible for the effect of motilin in both duodenectomized and normal dogs may involve a cholinergic pathway.The duodenum occupies a strategic anatomical position in the upper digestive tract and is intimately involved in the coordination of various functions of the upper gut. It influences gastric empting, 1 pancreatic and biliary secretion, 2 and the organization and initiation of gastric motor patterns 3,4 by invoking hormonal and neural mechanisms. Others have confirmed these findings.5-7 Tanaka and Sarr 8 reported that duodenectomy disrupts not only the coordination of gastric and intestinal migrating motor complexes (MMC) but also the coordination between interdigestive motility and pancreatic secretion, and it abolishes the interdigestive cyclic variations in plasma motilin and pancreatic polypeptide (PP) levels. 9 The release of PP appears to be regulated by a complex interplay between neural input (from the vagus) and humoral factors that originate from the upper gut. 10,11The duodenum also plays an important role by regulating the release of certain pancreatic hormones. For example, intraduodenal glucose administration causes the release of more insulin than does...

show abstract

“…Glucose tolerance Impaired glucose tolerance in some patients; reduced integrated incremental responses of gastric inhibitory polypeptide; delayed insulin and C-peptide responses; disrupted enteroinsular axis without significant overall reduction in integrated incremental responses. 174…”

Section: Resultsmentioning

confidence: 99%

Misoprostol Therapeutics Revisited

2001

View full text Add to dashboard Cite

Misoprostol, a prostaglandin E1 analog, is a racemate of four stereoisomers. On administration it rapidly de-esterifies to its active form, misoprostolic acid. Misoprostolic acid is 85% albumin bound and has a half-life of approximately 30 minutes. It is excreted in urine as inactive metabolites. No significant drug interactions have been reported. Besides its gastrointestinal protective and uterotonic activities, misoprostol regulates various immunologic cascades. It inhibits platelet-activating factor and leukocyte adherence, and modulates adhesion molecule expression. It protects against gut irradiation injury, experimental gastric cancer, enteropathy, and constipation. It improves nutrient absorption in cystic fibrosis. Misoprostol has utility in acetaminophen and ethanol hepatotoxicity, hepatitis, and fibrosis. It is effective in asthmatics and aspirin-sensitive asthmatic and allergic patients. It lowers cholesterol and severity of peripheral vascular diseases, prolongs survival of cardiac and kidney transplantation, synergizes cyclosporine, and protects against cyclosporine-induced renal damage. It works against drug-induced renal damage, interstitial cystitis, lupus nephritis, and hepatorenal syndrome. It is useful in periodontal disease and dental repair. Misoprostol enhances glycosoaminoglycan synthesis in cartilage after injury. It prevents ultraviolet-induced cataracts and reduces intraocular pressure in glaucoma and ocular hypertension. It synergizes antiinflammatory and analgesic effects of diclofenac or colchicine and has been administered to treat trigeminal neuralgic pain. It reduces chemotherapy-induced hair loss and recovery time from burn injury, and is effective in treating sepsis, multiple sclerosis, and pancreatitis.

show abstract

Effects of four orally administered analogues of prostaglandin E₁ and E₂ on glucose tolerance and on the secretion of pancreatic and gastrointestinal hormones in man

Cited by 8 publications

References 31 publications

Plasma and Tissue Hormones in the Dog after Administration of the Prostaglandin Analogue, Misoprostol

Plasma and Tissue Hormones in the Dog after Administration of the Prostaglandin Analogue, Misoprostol

Effect of Duodenectomy on Gastric Motility and Gastric Hormones in Dogs

Misoprostol Therapeutics Revisited

Contact Info

Product

Resources

About

Effects of four orally administered analogues of prostaglandin E1 and E2 on glucose tolerance and on the secretion of pancreatic and gastrointestinal hormones in man

Cited by 8 publications

References 31 publications

Plasma and Tissue Hormones in the Dog after Administration of the Prostaglandin Analogue, Misoprostol

Plasma and Tissue Hormones in the Dog after Administration of the Prostaglandin Analogue, Misoprostol

Effect of Duodenectomy on Gastric Motility and Gastric Hormones in Dogs

Misoprostol Therapeutics Revisited

Contact Info

Product

Resources

About

Effects of four orally administered analogues of prostaglandin E₁ and E₂ on glucose tolerance and on the secretion of pancreatic and gastrointestinal hormones in man