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

Maas, M.I.M.; Hopman, W. P. M.; Katan, Martijn B.; Jansen, J. B. M. J.

doi:10.1016/s0167-0115(96)00111-5

Cited by 7 publications

(10 citation statements)

References 57 publications

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“…In contrast to long-chain triglycerides, medium-chain triglycerides were unable to increase plasma cholecystokinin concentrations in healthy volunteers [29,30]. However, only infusion of cholecystokinin at high and probably supraphysiological doses inhibited gastrin-stimulated gastric acid secretion in humans, whereas plasma cholecystokinin increments within the physiological range were without a significant effect [8,29]. However, only infusion of cholecystokinin at high and probably supraphysiological doses inhibited gastrin-stimulated gastric acid secretion in humans, whereas plasma cholecystokinin increments within the physiological range were without a significant effect [8,29].…”

Section: Peptide Yy a Putative Enterogastronementioning

confidence: 63%

“…Previously, we have demonstrated that both long-chain triglycerides and medium-chain triglycerides are able to inhibit gastric acid secretion [29]. The inhibition was not mediated by circulating cholecystokinin as medium-chain triglycerides do not stimulate release of cholecystokinin into the plasma [30].…”

Section: Introductionmentioning

confidence: 82%

“…The inhibition was not mediated by circulating cholecystokinin as medium-chain triglycerides do not stimulate release of cholecystokinin into the plasma [30]. Furthermore, cholecystokinin infused into the plasma to concentrations somewhat higher than found during perfusion of the duodenum with long-chain triglycerides did not inhibit gastrin-stimulated gastric acid secretion [29]. Therefore, other hormones must be involved.…”

Section: Introductionmentioning

confidence: 84%

“…Recovery of gastric juice and the amount of acid secreted (mmol per 15 min) were calculated as described in our previous publication [29]. Subsequently, gastric samples were filtrated and alkalized with 2·5 mol L -1 NaOH and the concentration of phenol red was measured spectrophotometrically at 560 nm.…”

Section: Measurementsmentioning

confidence: 99%

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Release of peptide YY and inhibition of gastric acid secretion by long‐chain and medium‐chain triglycerides but not by sucrose polyester in men

Maas¹,

Hopman²,

Katan

et al. 1998

Eur J Clin Investigation

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Section: Peptide Yy a Putative Enterogastronementioning

confidence: 63%

Section: Introductionmentioning

confidence: 82%

Section: Introductionmentioning

confidence: 84%

Section: Measurementsmentioning

confidence: 99%

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Release of peptide YY and inhibition of gastric acid secretion by long‐chain and medium‐chain triglycerides but not by sucrose polyester in men

Maas¹,

Hopman²,

Katan

et al. 1998

Eur J Clin Investigation

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“…This might be the reason for the absence of plasma CCK secretion and suppression of gastric acid secretion in response to sucrose polyester. CCK may be involved in the suppression of gastric acid secretion by intraduodenal fat (18)(19)(20)(21)(22), although we showed that suppres sion of acid secretion can be reached by medium-chain triacylglycerols without concomitant CCK release (39). The in crease of plasma CCK in response to digestible fat was TABLE 1 Gastric acid output in (he stomach before gastrin infusion (basal), during gastrin infusion, and during intraduodenal perfusion of sucrose polyester (SPE), digestible fat, or saline in eight volunteers; intravenous gastrin infusion was continued during the intraduodenal perfusion of fat7 …”

mentioning

confidence: 58%

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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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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Physiological Effects of Medium-Chain Triglycerides: Potential Agents in the Prevention of Obesity

St‐Onge

Jones

2002

The Journal of Nutrition

296

200

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Medium chain fatty acids (MCFA) are readily oxidized in the liver. Animal and human studies have shown that the fast rate of oxidation of MCFA leads to greater energy expenditure (EE). Most animal studies have also demonstrated that the greater EE with MCFA relative to long-chain fatty acids (LCFA) results in less body weight gain and decreased size of fat depots after several months of consumption. Furthermore, both animal and human trials suggest a greater satiating effect of medium-chain triglycerides (MCT) compared with long-chain triglycerides (LCT). The aim of this review is to evaluate existing data describing the effects of MCT on EE and satiety and determine their potential efficacy as agents in the treatment of human obesity. Animal studies are summarized and human trials more systematically evaluated because the primary focus of this article is to examine the effects of MCT on human energy metabolism and satiety. Hormones including cholescytokinin, peptide YY, gastric inhibitory peptide, neurotensin and pancreatic polypeptide have been proposed to be involved in the mechanism by which MCT may induce satiety; however, the exact mechanisms have not been established. From the literature reviewed, we conclude that MCT increase energy expenditure, may result in faster satiety and facilitate weight control when included in the diet as a replacement for fats containing LCT.

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

Cited by 7 publications

References 57 publications

Release of peptide YY and inhibition of gastric acid secretion by long‐chain and medium‐chain triglycerides but not by sucrose polyester in men

Release of peptide YY and inhibition of gastric acid secretion by long‐chain and medium‐chain triglycerides but not by sucrose polyester in men

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

Physiological Effects of Medium-Chain Triglycerides: Potential Agents in the Prevention of Obesity

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