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/kgH2O), fructose (290 mosmol/kgH2O), aspartame (200 mg), and saccharin (50 mg); twice as sweet glucose ϩ 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 Ͻ 0.05). There was no additional effect of the sweeter glucose ϩ saccharin solution (P Ͼ 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 NUTRIENT-INDUCED GUT-TO-BRAIN signaling plays a major role in the control of mammalian digestive function, appetite, and energy intake (38). These effects are mediated by a number of interrelated factors, including the modulation of gastric emptying (GE) (46) and gastrointestinal transit (1,4,10,15,16), and the release from enteroendocrine cells of a number of signaling peptides, including glucagon-like peptide-1 (GLP-1) (17,23,24), peptide YY (PYY) (2, 32), and cholecystokinin (CCK) (35). These peptides signal to the central nervous system (CNS), particularly the brain stem and hypothalamus, via the vagus nerve and the bloodstream, and lead to the modulation of GE. However, although these target organ effects are well recognized, the precise sensing and signaling mechanism(s) by which the gut detects the chemical composition of ingested foods, and thereby induces signaling to the CNS to modulate gastrointestinal function and energy intake, are poorly defined.The GE of hexose sugars has traditionally been regarded to be dependent on the osmolality of the ingested test meal (9, 19). However, differences between the GE of equiosmolar solutions of glucose and fructose have been reported (9, 13, 31), suggesting that sugar(hexose)-specific effects also occur. Thus the role of osmolality may be overstated and ...