The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Effects of fat digestion on appetite, APD motility, and gut hormones in response to duodenal fat infusion in humans
Abstract
The presence of nutrients in the small intestine slows gastric emptying and suppresses appetite and food intake; these effects are partly mediated by the release of gut hormones, including CCK. We investigated the hypothesis that the modulation of antropyloroduodenal motility, suppression of appetite, and stimulation of CCK and glucagon-like peptide-1 secretion by intraduodenal fat are dependent on triglyceride hydrolysis by lipase. Sixteen healthy, young, lean men were studied twice in double-blind, randomized, crossover fashion. Ratings for appetite-related sensations, antropyloroduodenal motility, and plasma CCK and glucagon-like peptide-1 concentrations were measured during a 120-min duodenal infusion of a triglyceride emulsion (2.8 kcal/min) on one day with, on the other day without, 120 mg tetrahydrolipstatin, a potent lipase inhibitor. Immediately after the duodenal fat infusion, food intake at a buffet lunch was quantified. Lipase inhibition with tetrahydrolipstatin was associated with reductions in tonic and phasic pyloric pressures, increased numbers of isolated antral and duodenal pressure waves, and stimulation of antropyloroduodenal pressure-wave sequences (all P < 0.05). Scores for prospective consumption and food intake at lunch were greater, and nausea scores were slightly less, and the rises in plasma CCK and glucagon-like peptide-1 were abolished (all P < 0.05). In conclusion, lipase inhibition attenuates the effects of duodenal fat on antropyloroduodenal motility, appetite, and CCK and glucagon-like peptide-1 secretion.
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Cites
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“Therefore, it is possible that some patients taking THL increase their energy intake (28), although the latter has not been formally evaluated in these chronic studies (7, 25).”
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“Therefore, it is possible that some patients taking THL increase their energy intake (28), although the latter has not been formally evaluated in these chronic studies (7, 25).”
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Cited by
Steinert, R. E., Feinle-Bisset, C., Asarian, L., Horowitz, M., Beglinger, C., & Geary, N. (2017) · Physiological Reviews · doi:10.1152/physrev.00031.2014 · Cited by 578
Self-citationIleal brake: a sensible food target for appetite control. A review
Maljaars, P. W. J., Peters, H. P. F., Mela, D. J., & Masclee, A. A. M. (2008) · Physiology & Behavior · doi:10.1016/j.physbeh.2008.07.018 · Cited by 451
The physiological roles of dietary fibre
Brownlee, I. A. (2011) · Food Hydrocolloids · doi:10.1016/j.foodhyd.2009.11.013 · Cited by 417
Gentilcore, D., Chaikomin, R., Jones, K. L., Russo, A., Feinle-Bisset, C., Wishart, J. M., Rayner, C. K., & Horowitz, M. (2006) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2005-2644 · Cited by 351
Self-citationGlucagon-like peptide 1(GLP-1) in biology and pathology
Meier, J. J., & Nauck, M. A. (2005) · Diabetes/Metabolism Research and Reviews · doi:10.1002/dmrr.538 · Cited by 288
Metadata
- Authors
- Feinle, C., O'Donovan, D., Doran, S., Andrews, J. M., Wishart, J., Chapman, I., & Horowitz, M.
- Venue
- American Journal of Physiology-Gastrointestinal and Liver Physiology
- Publisher
- American Physiological Society
- Published
- 2003-05-01
- Volume
- 284
- Issue
- 5
- Pages
- G798-G807
- ISSN
- 0193-1857 (ISSN-L)
- 1522-1547
- OpenAlex
- W2099767750
- Cited by
- 198
- References
- 5
- FWCI
- 3.98
- Type
- journal article
- Language
- en
- Open access
- closed
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- Feinle, C., O'Donovan, D., Doran, S., Andrews, J. M., Wishart, J., Chapman, I., & Horowitz, M. (2003). Effects of fat digestion on appetite, APD motility, and gut hormones in response to duodenal fat infusion in humans. American Journal of Physiology-Gastrointestinal and Liver Physiology. https://doi.org/10.1152/ajpgi.00512.2002
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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