Neural modulation of triglyceride-stimulated cholecystokinin release in dogs

Lilja, Per; Wiener, Isidoro; Greeley, George H.; Thompson, J.C.

doi:10.1016/0167-0115(83)90909-6

Cited by 2 publications

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“…Since the dose of atropine used is known to inhibit gastric emptying [11], it is impossible to conclude whether this impaired CCK re lease results from a direct inhibition of CCK secretion by atropine or from a reduced intraduodcnal load of fat due to slow gastric emptying. Lilja et al [10] reported that ad ministration of atropine inhibited the plasma CCK response to intraduodenal corn oil in dogs. Since these workers measured the plasma CCK concentrations for only 60 min, it cannot be derived from that study whether atropine inhibited or delayed the plasma CCK response to intraduodenal fat.…”

Section: Discussionmentioning

confidence: 99%

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Effect of Atropine on the Plasma Cholecystokinin Response to Intraduodenal Fat in Man

Hopman

Jansen

Lamers³

1984

Digestion

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The present study was undertaken to determine whether atropine inhibits the plasma cholecystokinin (CCK) response to intraduodenal fat. Plasma CCK concentrations were measured by radioimmunoassay using two sequence-specific antibodies. Antibody 1703 bound to all COOH-terminal CCK peptides containing at least 14 amino acid residues, while antibody T204 was specific for the sulphated tyrosine region of CCK. Intraduodenal instillation of 60 ml corn oil in 6 normal subjects induced significant increases in plasma CCK. Intravenous administration of atropine (0.015 mg/kg as bolus followed by 0.005 mg/kg · h over 3 h) resulted in significant inhibition of plasma CCK concentrations at 10, 20 and 30 min (antibody 1703) and at 20 and 30 min (antibody T204) after instillation of fat. However, the peak increments in plasma CCK during atropine (8.6 ± 1.9 pmol/l, antibody 1703; 5.4 ± 1.1 pmol/l, antibody T204) were not different from those found without atropine (6.3 ± 0.8 pmol/l, antibody 1703; 3.9 ± 0.9 pmol/l, antibody T204). Similarly, the integrated plasma CCK secretion after intraduodenal fat was not significantly different when measured during atropine (461 ± 119 pmol/l·3 h, antibody 1703; 269 ± 97 pmol/l·3 h, antibody T204) and without atropine (428 ± 62 pmol/l·3 h, antibody 1703; 188 ± 66 pmol/l·3 h).It is concluded that administration of atropine delays but does not inhibit the CCK response to intraduodenal corn oil in man.

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Section: Discussionmentioning

confidence: 99%

“…In two recent studies, reported in abstract form, the effect of atropine on fat-stimulated plasma CCK secretion was measured by ra dioimmunoassay [9,10]. Maton et al [9] showed that administration of atropine in hibited the plasma CCK response to oral fat.…”

Section: Discussionmentioning

confidence: 99%

Effect of Atropine on the Plasma Cholecystokinin Response to Intraduodenal Fat in Man

Hopman

Jansen

Lamers³

1984

Digestion

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Atropine-Nonsensitive Feedback Regulatory Mechanism of Rat Pancreatic Enzyme Secretion in Response to Food Protein Intake

Fushiki

Fukuoka

Kajkira

et al. 1987

The Journal of Nutrition

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The effect of atropine on pancreatic enzyme secretion in response to removal of intraluminal protease was investigated using rats with an indwelling bile-pancreatic cannula. Stimulation of pancreatic enzyme secretion by diversion of bile-pancreatic juice was blocked by intravenous atropine [100 micrograms/(kg X h)] injection. On the other hand, stimulation of pancreatic enzyme secretion by intraluminal infusion of soybean trypsin inhibitor (SBTI) was not blocked by atropine administration. These results suggest that the feedback response of pancreatic enzyme secretion after removal of the intraluminal protease is controlled by at least two different systems, an atropine-sensitive mechanism and an atropine-nonsensitive mechanism. We detected and purified a peptide from rat bile-pancreatic juice that enhanced pancreatic enzyme secretion when the peptide was infused into the proximal intestine. In the atropine-administered rat whose small intestine was deprived of protease after intraluminal washing with saline containing SBTI, intraluminal infusion of the purified peptide stimulated pancreatic enzyme secretion markedly. These findings suggest that the atropine-nonsensitive feedback response of pancreatic enzyme secretion is at least in part mediated by the peptide.

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Neural modulation of triglyceride-stimulated cholecystokinin release in dogs

Cited by 2 publications

References 0 publications

Effect of Atropine on the Plasma Cholecystokinin Response to Intraduodenal Fat in Man

Effect of Atropine on the Plasma Cholecystokinin Response to Intraduodenal Fat in Man

Atropine-Nonsensitive Feedback Regulatory Mechanism of Rat Pancreatic Enzyme Secretion in Response to Food Protein Intake

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