Effect of bile salt binding or protease inactivation on plasma cholecystokinin and gallbladder responses to bombesin

Replacement of dietary lilt by sucrose polyester reduces fat intake. However, little is known about the effccts of sucrose polyester on gastrointestinal function. To investigate the effect on gastric acid secretion and on release of cholecystokinin into plasma, we perfused eight healthy male volunteers intraduodenally with sucrose polyester, digestible fat, or saline on separate days in random order, Intraduodenal perfusion of sucrose polyester did not suppress gastrin-stimulated gastric acid secretion ( -1.8 ± 6,8%) whereas digestible fat suppressed gastric acid secretion by 64 ± 9% (P = 0.001) compared with saline. Sucrose polyester did not affect plasma cholecystokinin concentrations (-12.8 ± 9.3 pmol • 30 min/L) whereas perfusion with digestible fat resulted in a significant increase (31.7 ± 9.3 pmol -30 min/L, P ~ 0,017) compared with saline. We conclude that sucrose polyester, in contrast with digestible fat, does not inhibit gastrin-stimulated gastric acid secretion or stimulate release of cholecystokinin, KEY WORDS cholecystokininGastric acid secretion, sucrose polyester, Stimulation of plasma CCK and pancreaticobiliary secretion by fatty nutrients depends on the presence of the products of fat digestion in the proximal small intestine (23-29). The inhibi tion of gastric acid secretion by fat might dopend on (he digestion of fat as well.We report the effect of digestible fat and the indigestible fat sucrose polyester on gastric acid secretion and on CCK release in men.

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“…Plasma gastrin and CCK concentrations were measured by sensitive and specific radioimmunoassays as described previ ously (32)(33)(34)(35) …”

Section: Experimental Designmentioning

confidence: 99%

Sucrose polyester does not inhibit gastric acid secretion or stimulate cholecystokinin release in men

Maas

Hopman

Wijk

et al. 1997

The American Journal of Clinical Nutrition

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“…The catheters acid secreted (m m o l/15 min) was calculated as follows: were kept patent by a heparin-saline solution. One catheter (acid concentration measured) X /recovery, was used for the collection of blood samples and the other Gastrin, CCK and PP concentrations in" plasma were for the infusion of non-sulphated gastrin-17 at a dose of 10 measured by sensitive and specific radioimmunoassays as pm ol/kg per h. This dose produces plasma gastrin concenpreviously described [16][17][18][19]. trations similar to those found after a meal [15].…”

Section: G Astrinmentioning

confidence: 99%

Inhibition of gastrin-stimulated gastric acid secretion by medium-chain triglycerides and long-chain triglycerides in healthy young men

Maas¹,

Hopman²,

Katan³

et al. 1996

Regulatory Peptides

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Long-chain triglycerides inhibit gastric acid secretion, but the effect of medium-chain triglycerides in humans is unknown. We compared the effects of intraduodenally perfused saline, medium-chain and long-chain triglycerides on gastrin-stimulated gastric acid secretion and cholecystokinin release. Eight healthy male volunteers participated in this study. Gastrin-stimulated gastric acid output was 9.4 ± 1.1 m m ol/30 min during saline perfusion. It was suppressed by medium-chain triglycerides by 43 ± 9% (P = 0.04 vs. saline) and by long-chain triglycerides by 74 ± 6% (P -0.0003 vs. saline). Thus medium-chain triglycerides inhibited gastrin-stimulated gastric acid secretion but less so than long-chain triglycerides. When compared to saline perfusion (73 ± 6 pM X 30 min) integrated plasma cholecystokinin concentrations were significantly elevated by long-chain triglycerides (96 ±5 pM X 30 min, P < 0,004) but not by medium-chain triglycerides perfusion (65 ± 7 pM X 30 min). We also investigated the role of cholecystokinin infusion on gastrin stimulated gastric acid secretion. Higher concentrations (191.4 ± 4,5 pM X 30 min) of CCK than released in the long-chain triglycerides perfusion experiment, did not suppress gastric acid secretion. Thus, circulating cholecystokinin appears not responsible for the inhibition of gastrin-stimulated gastric acid secretion by dietary fat.

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“…Direct effects of cholestyramine on these functions are unlikely, since colestipol, a bile salt-binding resin with a different molecular structure from cholestyramine, has comparable effects on CCK release and gallbladder motility (5). Nevertheless» cholestyramine may indirectly affect gallbladder motility and plasma CCK release by enhancing gastric emptying (6) or by delaying the digestion of fatty nutrients (1).…”

mentioning

confidence: 99%

“…In physiologic studies that used cholestyramine to pre cipitate bile acids, cholestyramine enhanced plasma CCK levels and gallbladder responses to an orally or intraduodenally administered mixed meal (1)(2)(3)(4) and to bombesin infusion (5). Direct effects of cholestyramine on these functions are unlikely, since colestipol, a bile salt-binding resin with a different molecular structure from cholestyramine, has comparable effects on CCK release and gallbladder motility (5).…”

mentioning

confidence: 99%

“…Cholestyramine is a drug used in clinical practice to lower plasma cholesterol levels, to treat obstructive liver diseases, or to decrease diarrhoea induced by bile salt overflow into the colon. Recently, cholestyramine has also been used as a tool in physiologic studies to investigate the role of bile salts in the regulation of plasma cholecystokinin (CCK) release and pancreaticobiliary secretion (1)(2)(3)(4)(5).…”

mentioning

confidence: 99%

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Cholestyramine Influences Meal-Stimulated Pancreaticobiliary Function and Plasma Cholecystokinin Independent of Gastric Emptying and Food Digestion

Thimister

Hopman

Loualidi

et al. 1997

Scandinavian Journal of Gastroenterology

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Thimister PWL, Hopman WPM, Loualidi A, Rosenbusch G, Willems HL, Trijbels FJM, Jansen JBMJ. Cholestyramine influences meal-stimulated pancreaticobiliary function and plasma cholecystokinin independent of gastric emptying and food digestion. Scand J Gastroenterol 1997;32:778-784.Background: Cholestyramine enhances gallbladder emptying and plasma cholecystokinin responses to oral ingestion of a mixed meal. It is not known whether this effect occurs independently of alterations in gastric emptying or maldigestion of nutrients. Methods: We perfused 15 g of an amino acid meal intraduodenally for 60 min in seven healthy volunteers, once with and once without cholestyramine, Intraduodenal perfusion of saline with or without cholestyramine (6 g/h) was started 60 min before the amino acid meal and continued for 2h. Results: Cholestyramine markedly enhanced the incremental plasma cholecystokinin response to the meal from 36 ± 12 to 139 ± 25pmol/1 -60min (P < 0.005), incremental amylase output from 2.4 ± 0.7 to 5.7 ± 0.7 kU/h (.P < 0.05), and incremental integrated gallbladder contraction from 1948 ± 235 to 2840 ± 189% * 60 min (P < 0.05). Conclusion: The enhanc ing effect of cholestyramine on postprandial gallbladder contraction, pancreatic enzyme secretion, and plasma cholecystokinin release is not dependent on gastric emptying rates or appropriate digestion of nutrients.

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Effect of bile salt binding or protease inactivation on plasma cholecystokinin and gallbladder responses to bombesin

Cited by 20 publications

References 43 publications

Sucrose polyester does not inhibit gastric acid secretion or stimulate cholecystokinin release in men

Sucrose polyester does not inhibit gastric acid secretion or stimulate cholecystokinin release in men

Inhibition of gastrin-stimulated gastric acid secretion by medium-chain triglycerides and long-chain triglycerides in healthy young men

Cholestyramine Influences Meal-Stimulated Pancreaticobiliary Function and Plasma Cholecystokinin Independent of Gastric Emptying and Food Digestion

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