Sweetness and bitterness taste of meals per se does not mediate gastric emptying in humans

1 Section of Gastrointestinal Sciences, Manchester Academic Health Science Centre, University of Manchester, Salford Royal National Health Service Foundation Trust, Salford; and 2 University of Manchester, Faculty of Life Sciences, Manchester, United Kingdom Submitted 10 February 2009 ; accepted in...

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Published inAmerican journal of physiology. Regulatory, integrative and comparative physiology Vol. 297; no. 3; pp. R632 - R639
Main Authors Little, Tanya J, Gupta, Nili, Case, R. Maynard, Thompson, David G, McLaughlin, John T
Format Journal Article
LanguageEnglish
Published United States American Physiological Society 01.09.2009
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ISSN0363-6119
1522-1490
1522-1490
DOI10.1152/ajpregu.00090.2009

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Summary:1 Section of Gastrointestinal Sciences, Manchester Academic Health Science Centre, University of Manchester, Salford Royal National Health Service Foundation Trust, Salford; and 2 University of Manchester, Faculty of Life Sciences, Manchester, United Kingdom Submitted 10 February 2009 ; accepted in final form 11 June 2009 In cell line and animal models, sweet and bitter tastants induce secretion of signaling peptides (e.g., glucagon-like peptide-1 and cholecystokinin) and slow gastric emptying (GE). Whether human GE and appetite responses are regulated by the sweetness or bitterness per se of ingested food is, however, unknown. We aimed to determine whether intragastric infusion of "equisweet" ( Study A ) or "equibitter" ( Study B ) solutions slow GE to the same extent, and whether a glucose solution made sweeter by the addition of saccharin will slow GE more potently than glucose alone. Healthy nonobese subjects were studied in a single-blind, randomized fashion. Subjects received 500-ml intragastric infusions of predetermined equisweet solutions of glucose (560 mosmol/kgH 2 O), fructose (290 mosmol/kgH 2 O), aspartame (200 mg), and saccharin (50 mg); twice as sweet glucose + saccharin, water (volumetric control) ( Study A ); or equibitter solutions of quinine (0.198 mM), naringin (1 mM), or water ( Study B ). GE was evaluated using a [ 13 C]acetate breath test, and hunger and fullness were scored using visual analog scales. In Study A , equisweet solutions did not empty similarly. Fructose, aspartame, and saccharin did not slow GE compared with water, but glucose did ( P < 0.05). There was no additional effect of the sweeter glucose + saccharin solution ( P > 0.05, compared with glucose alone). In Study B , neither bitter tastant slowed GE compared with water. None of the solutions modulated perceptions of hunger or fullness. We conclude that, in humans, the presence of sweetness and bitterness taste per se in ingested solutions does not appear to signal to influence GE or appetite perceptions. taste; gastrointestinal tract; bitter; sweet Address for reprint requests and other correspondence: T. Little, Univ. of Manchester, Section of Gastrointestinal Sciences, Clinical Sciences Bldg., Salford Royal NHS Foundation Trust, Stott Lane, Salford, United Kingdom, M6 8HD (e-mail: tanya.little{at}adelaide.edu.au )
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Address for reprint requests and other correspondence: T. Little, Univ. of Manchester, Section of Gastrointestinal Sciences, Clinical Sciences Bldg., Salford Royal NHS Foundation Trust, Stott Lane, Salford, United Kingdom, M6 8HD (e-mail: tanya.little@adelaide.edu.au)
ISSN:0363-6119
1522-1490
1522-1490
DOI:10.1152/ajpregu.00090.2009