Cholecystokinin-Like Activities in Guinea Pigs and in Dogs of the C-Terminal Octapeptide (SQ 19,844) of Cholecystokinin

Rubin, Bernard; Engel, Stanford L.; Drungis, A.M.; Dzelzkalns, Margaret; Grigas, Eleanor O.; Waugh, Margaret H.; Yiacas, Euripides

doi:10.1002/jps.2600580810

Cited by 56 publications

(12 citation statements)

References 17 publications

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“…The lower esophageal sphincter contracts in response to gastrin (12)(13)(14) whereas both the ileocecal (15) and choledochal sphincters (16) (25) and suggested that contaminants present in the GIH Research Unit preparation of cholecystokinin were not solely responsible for the observed response (26)(27)(28).…”

Section: Discussionmentioning

confidence: 99%

The Hormonal Regulation of Pyloric Sphincter Function

Fisher¹,

Lipshutz²,

Cohen³

1973

J. Clin. Invest.

120

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A B S T R A C T The purpose of this study was to evaluate the hormonal control of pyloric sphincter function. Studies were performed on both pyloric circular muscle, in vitro, and the human pylorus, in vivo. Full dose-response curves to gastrin I, cholecystokinin, and secretin were constructed for the pyloric muscle of the opossum studied at its length of optimal tension development, Lo. Both cholecystokinin and secretin were potent agonists on the muscle but gastrin I gave no increase in muscle tension. The combination of cholecystokinin and secretin was additive at submaximal concentrations but potentiation of the maximal responses was not observed. Gastrin I produced a surmountable, competitive-like antagonism to the effect of cholecystokinin on the pyloric muscle. The octapeptide of cholecystokinin was a more potent agonist than the whole molecule of cholecystokinin on the pyloric muscle. In man, the pyloric pressure rose significantly during intravenous infusion of either cholecystokinin or secretin. The combination of maximal doses of both hormones did not show signficant potentiation. Gastrin I did not significantly increase pyloric pressure but did antagonize the pyloric response to duodenal acidification. These studies suggest that: (a) Both secretin and cholecystokinin augment pyloric sphincter pressure while gastrin I is an antagonist inhibiting their effects. (b) The hormonal responses of pyloric sphincter circular muscle, in vitro, can be correlated with human sphincter function, in vivo.

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Section: Discussionmentioning

confidence: 99%

The Hormonal Regulation of Pyloric Sphincter Function

Fisher¹,

Lipshutz²,

Cohen³

1973

J. Clin. Invest.

120

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“…It is well established that the COOHterminal heptapeptide amide of CCK contains all the information needed for biological activity (1). Moreover, CCK8 has been shown to be 2-10 times more potent on a molar basis than CCK33 or CCK39 in several systems including stimulation of gall bladder contraction in vivo and in vitro, and stimulation of pancreatic enzyme secretion in vivo (5)(6)(7). The possibility arises then, that an imbalance in the amount or type of CCK could contribute to pancreatic or gall bladder malfunction.…”

Section: Introductionmentioning

confidence: 99%

Identification and measurement of molecular variants of cholecystokinin in duodenal mucosa and plasma. Diminished concentrations in patients with celiac disease.

Calam¹,

Ellis²,

Dockray³

1982

J. Clin. Invest.

151

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A B S T R A C T The amount and type of cholecystokinin (CCK) in duodenal extracts and plasma of celiac patients and normal subjects was studied by radioimmunoassay and gel filtration. In both groups there were similar patterns of molecular forms in extracts of duodenal biopsies, but concentrations in celiac disease were significantly depressed. In boiling water extracts of duodenal mucosa from both groups a factor with the properties of the COOH-terminal octapeptide of cholecystokinin predominated, but there were also significant amounts of a larger molecular weight form. In acid extracts of mucosa a factor with the properties of the 33 or 39 residue form was identified in amounts that were -25% those of CCK8; there were also similar amounts of an acid-soluble form that had an apparent molecular weight higher than CCK39. Plasma immunoreactive cholecystokinin was studied after concentration by immunoaffinity adsorption and fractionation by gel filtration. In normal subjects fasting CCK-like immunoreactivity was <0.8 pmol/liter, and after a light breakfast increased to 2.0±0.7(range 1.0 to 4.8) pmol/liter; CCK8-like activity accounted for all the increased immunoreactivity. In five of six celiac patients the concentrations of both fasting and postprandial CCK-like immunoreactivity in plasma were undetectable (<0.8 pmol/liter). We conclude that diminished production and release of CCK could account for the impaired pancreatic and gall bladder responses to intraluminal stimuli in celiac disease.

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“…The suppression of food intake by this preparation was a property of the CCK molecule and was not due to impurities present in the extract, because the synthetic C-terminal octapeptide of CCK and the decapeptide caerulein suppressed food intake (Experiment 2). Both the octapeptide (Rubin, Engel, Drungis, Dzelzkalns, Grigas, Waugh, & Yiacas, 1969) and caerulein (Stening & Grossman, 1969a;Stening, Johnson, & Grossman,. 1969;Vagne & Grossman, 1968) have the physiological spectrum of action of the whole CCK molecule.…”

Section: Discussionmentioning

confidence: 99%

Cholecystokinin Decreases Food Intake in Rats¹

1997

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Partially purified cholecystokinin (CCK) was injected intraperitoneally into fasted rats prior to food presentation. The hormone produced a large dose-related suppression of intake of solid and liquid diets. Identical doses of the synthetic terminal octapeptide of cholecystokinin produced identical results. An effective dose of CCK did not suppress drinking after water deprivation. Treated animals did not appear ill and were not hyperthermic; neither CCK nor the octapeptide produced learning of a taste aversion in bait-shyness tests. The effect of CCK is not a property of all gut hormones, since injections of secretin did not affect feeding. These studies raise the possibility that CCK plays an inhibitory role in the short-term control of feeding behavior.

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Cholecystokinin-Like Activities in Guinea Pigs and in Dogs of the C-Terminal Octapeptide (SQ 19,844) of Cholecystokinin

Cited by 56 publications

References 17 publications

The Hormonal Regulation of Pyloric Sphincter Function

The Hormonal Regulation of Pyloric Sphincter Function

Identification and measurement of molecular variants of cholecystokinin in duodenal mucosa and plasma. Diminished concentrations in patients with celiac disease.

Cholecystokinin Decreases Food Intake in Rats¹

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Cholecystokinin-Like Activities in Guinea Pigs and in Dogs of the C-Terminal Octapeptide (SQ 19,844) of Cholecystokinin

Cited by 56 publications

References 17 publications

The Hormonal Regulation of Pyloric Sphincter Function

The Hormonal Regulation of Pyloric Sphincter Function

Identification and measurement of molecular variants of cholecystokinin in duodenal mucosa and plasma. Diminished concentrations in patients with celiac disease.

Cholecystokinin Decreases Food Intake in Rats1

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Cholecystokinin Decreases Food Intake in Rats¹