Little TJ, Gupta N, Case RM, Thompson DG, McLaughlin JT
Sweetness and bitterness taste of meals per se does not mediate gastric emptying in humans. [JOURNAL ARTICLE]
Am J Physiol Regul Integr Comp Physiol 2009 Jun 17.
Background: In cell line and animal models sweet and bitter tastants induce secretion of signaling peptides (e.g. GLP-1 and CCK) and slow gastric emptying (GE). Whether human GE and appetite responses are regulated by the sweetness or bitterness per se or ingested food is, however, unknown.
Aims: To determine whether intragastric infusion of "equi-sweet" (Study A) or "equi-bitter" (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.
Methods: Healthy non-obese subjects were studied in a single-blind, randomized fashion. Subjects received 500 ml intragastric infusions of pre-determined "equi-sweet" solutions of glucose (560 mOsmol), fructose (290 mOsmol), aspartame (200 mg), saccharin (50 mg); twice as sweet glucose+saccharin, or water (volumetric control) (Study A), or "equi-bitter" solutions of quinine (0.198 mM), naringin (1 mM), or water (Study B). GE was evaluated using a 13C-acetate breath test, and hunger and fullness scored using visual analogue scales.
Results: Study A: Equi-sweet solutions did not empty similarly. Fructose, aspartame and saccharin did not slow GE compared to 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). Study B: Neither bitter tastant slowed GE compared with water. None of the solutions modulated perceptions of hunger or fullness.
Conclusions: In man, the presence of sweetness and bitterness taste per se in ingested solutions does not appear to signal to influence GE or appetite perceptions. Key words: taste, gastrointestinal tract, sweet, bitter.
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