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Am J Physiol Gastrointest Liver Physiol (March 1, 2007). doi:10.1152/ajpgi.00452.2006
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Submitted on September 30, 2006
Accepted on February 27, 2007

Enhancement of intragastric acid stability of a fat emulsion meal delays gastric emptying, increases cholecystokinin release and gallbladder contraction

Luca Marciani1, Martin Wickham2, Gulzar Singh3, Debbie Bush4, Barbara Pick4, Eleanor Cox5, Annette Fillery-Travis2, Richard Faulks2, Charles Marsden3, Penny A Gowland5, and Robin Spiller6*

1 Wolfson Digestive Diseases Centre, University of Nottingham, Nottingham, United Kingdom
2 Institute of Food Research, Norwich, United Kingdom
3 School of Biomedical Sciences, University of Nottingham, Nottingham, United Kingdom
4 Division of Surgery, University of Nottingham, Nottingham, United Kingdom
5 Sir Peter Mansfield Magnetic Resonance Centre, Univeristy of Nottingham, Nottingham, United Kingdom
6 University of Nottingham, United States; Wolfson Digestive Diseases Centre, University of Nottingham, Nottingham, United Kingdom; University of Nottingham

* To whom correspondence should be addressed. E-mail: robin.spiller{at}nottingham.ac.uk.

Pre-processed fatty foods often contain calories added as a fat emulsion stabilised by emulsifiers. Emulsion stability in the acidic gastric environment can readily be manipulated by altering emulsifier chemistry. We tested the hypothesis that it would be possible to control gastric emptying, cholecystokinin (CCK) release and satiety by varying intragastric fat emulsion stability. Nine healthy volunteers received a test meal on 2 occasions, comprising a 500 ml 15% oil emulsion with 2.5% of one of two emulsifiers that produced emulsions which were either stable (meal A) or unstable (meal B) in the acid gastric environment. Gastric emptying and gallbladder volume changes were assessed using magnetic resonance imaging. CCK plasma levels were measured and satiety scores were recorded. Meal B layered rapidly due to fat emulsion breakdown. The gastric half-emptying time of the aqueous phase was faster for meal B (72±13 min) than for meal A (171±35 min, P<0.008). Meal A released more CCK than meal B (integrated areas respectively 1095±244 and 531±111 pmol.min/L, P<0.02), induced a greater gallbladder contraction (P<0.02) and decreased post-prandial appetite (P<0.05) although no significant differences were observed in fullness and hunger. We conclude that acid-stable emulsions delayed gastric emptying, increased postprandial CCK levels and gallbladder contraction, while acid-instability led to rapid layering of fat in the gastric lumen with accelerated gastric emptying, lower CCK levels and reduced gallbladder contraction. Manipulation of the acid stability of fat emulsion added to pre-processed foods could maximise satiety signalling and, in turn, help to reduce overconsumption of calories.







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