Effect of Atropine on Intestinal Phase of Pancreatic Secretion in Man

Bozkurt, T; Adler, Guido; Koop, Irmtraut; Arnold, R.

doi:10.1159/000199739

Cited by 33 publications

(17 citation statements)

References 11 publications

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“…Unfortunately, in that study, the CCK preparation used was impure and there were no determinations of plasma CCK made in their investigation, therefore, no assessment of physiological relevance could be made. More recently we (5) and others (6,7) have shown that, in humans, CCK infusion that produced plasma CCK levels similar to those seen postprandially stimulated pancreatic secretion by an atropine-sensitive pathway. These observations suggest that in both humans and experimental animals cholinergic neural pathways rather than pancreatic acini represent the primary targets in which CCK acts to stimulate pancreatic enzyme secretion.…”

Section: Discussionmentioning

confidence: 65%

Vagal afferent pathway mediates physiological action of cholecystokinin on pancreatic enzyme secretion.

Li¹,

Owyang²

1993

J. Clin. Invest.

181

133

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To establish the mechanism(s) and site(s) of action of cholecystokinin (CCK) on pancreatic secretion under physiological conditions, we used an in vivo model using anesthetized rats with pancreaticobiliary cannulas. Infusion of CCK-8 (10-160 pmol/kg per h) produced a dose-dependent increase in plasma CCK levels. CCK-8 infusion at 40 pmol/kg per h produced a plasma CCK level of7.9±1.5 pM and an80% increase in pancreatic protein output over basal. This level was closely approximated by a postprandial peak plasma CCK level by 6.2±1.

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Section: Discussionmentioning

confidence: 65%

Vagal afferent pathway mediates physiological action of cholecystokinin on pancreatic enzyme secretion.

Li¹,

Owyang²

1993

J. Clin. Invest.

181

133

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“…1) after protein administration, loxiglumide did not alter C-peptide responses or estimated insulin secretion rates. C-peptide can be used to accu rately estimate insulin secretion in vivo [24,29,30], It should be noted that, as described pre viously [31], with the intraduodenal nutrient stimulation used, rather high plasma CCK concentrations were found in comparison to those values usually found after orally in gested meals, and that 'normal' postprandial CCK concentrations (approximately 3-8 pmol/1) [21,32] are even less likely to have an influence on insulin secretion.…”

Section: Discussionmentioning

confidence: 99%

Role of Endogenously Released Cholecystokinin in Determining Postprandial Insulin Levels in Man: Effects of Loxiglumide, a Specific Cholecystokinin Receptor Antagonist

Baum¹,

Ebert²,

Cantor

et al. 1992

Digestion

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To estimate the contribution of postprandial cholecystokinin (CCK) responses to circulating insulin concentrations and insulin secretion, a specific CCK receptor antagonist (loxiglumide; 10 mg/kg body weight/h) or saline were infused intravenously in normal volunteers, beginning 90 min before insulin secretion was stimulated on separate occasions by the intraduodenal administrations of glucose, glucose and protein, and glucose plus protein with the admixture of pancreatin. The release of CCK (radioimmunoassay) was stimulated by the protein component of the nutrients from basal 2.4 ± 0.4 to 8.0 ± 1.2 pmol/l. CCK plasma levels were significantly higher with loxiglumide (p < 0.05). Glucose-dependent insulinotropic polypeptide (GIP) was also released by all nutrient mixtures. Loxiglumide significantly inhibited the amount of bilirubin and pancreatic enzymes recovered from duodenal aspirates. In contrast, in none of the experiments, C-peptide increments and hence insulin secretion rates were altered by loxiglumide. With glucose and protein as intraduodenal stimulus (no pancreatin added), the plasma amino acids rose significantly less (by approximately 50% of the control experiment) and the increment in insulin (but not C-peptide) concentrations was significantly reduced by loxiglumide. This is most likely explained by a change in insulin metabolic clearance. This effect cannot be a primary action of CCK because there was no similar effect of loxiglumide with the same intraduodenal stimulus plus added pancreatin. Pancreatic enzymes reduced maldigestion secondary to loxiglumide effects on pancreatic exocrine secretion: The increment in circulating amino acid concentrations was similar with and without loxiglumide. In conclusion, CCK does not alter insulin secretion and, therefore, is not an incretin hormone in man. Blocking CCK actions on the exocrine pancreas by loxiglumide, however, can secondarily cause reductions in postprandial insulin profiles by altering insulin clearance. These changes are possibly related to reductions in circulating amino acid concentrations.

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“…Both found that the secretory re sponse to a liquid lest meal averaged 50 60% of maximal capacity. Data from our own laboratory have shown that oral intake of a liquid lest meal produces a comparable response to that obtained by perfusing the same meal into the duodenum [17], Perfusion of individual nutrients to the duodenum induces different quantities of enzymes. Carbohydrates have little effect, amino acids an inter mediate effect, and fat causes maximal enzyme output [18], Di Magno and Layer [19] demonstrated that the secretory response of the pancreas depends on when one eats during the interdigestive cycle.…”

Section: Intestinal Phasementioning

confidence: 91%

Regulation of Human Pancreatic Secretion

Adler

1997

Digestion

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Effect of Atropine on Intestinal Phase of Pancreatic Secretion in Man

Cited by 33 publications

References 11 publications

Vagal afferent pathway mediates physiological action of cholecystokinin on pancreatic enzyme secretion.

Vagal afferent pathway mediates physiological action of cholecystokinin on pancreatic enzyme secretion.

Role of Endogenously Released Cholecystokinin in Determining Postprandial Insulin Levels in Man: Effects of Loxiglumide, a Specific Cholecystokinin Receptor Antagonist

Regulation of Human Pancreatic Secretion

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