scholarly journals Extinction of the consummatory response to a saccharin solution

1968 ◽  
Vol 10 (2) ◽  
pp. 81-82 ◽  
Author(s):  
Ray Foster
1960 ◽  
Vol 6 (3) ◽  
pp. 327-331 ◽  
Author(s):  
Maurice Korman ◽  
Harold D. Stephens

1964 ◽  
Vol 14 (2) ◽  
pp. 507-512 ◽  
Author(s):  
William A. McLaurin ◽  
John A. Farley ◽  
Barron B. Scarborough ◽  
Travis D. Rawlings

Two separate studies were made to determine the degree of post-irradiation saccharin avoidance behavior displayed by rats given tap water or no fluid to drink prior to low-level x-irradiation exposure. In neither study were significant differences, in post-treatment saccharin avoidance behavior, found between the groups receiving saccharin solution, tap water or no fluid to drink prior to radiation exposure. It was concluded that the results could be viewed as additional evidence for the hypothesis of an association of a disturbed physiological state and the discriminatory saccharin solution in the home cage and not an association of x-irradiation with saccharin solution per se. Doubt was expressed that the results could be taken as evidence for successful backward conditioning.


2009 ◽  
Vol 297 (3) ◽  
pp. R632-R639 ◽  
Author(s):  
Tanya J. Little ◽  
Nili Gupta ◽  
R. Maynard Case ◽  
David G. Thompson ◽  
John T. McLaughlin

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 + 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 [13C]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.


1971 ◽  
Vol 23 (1) ◽  
pp. 3-4 ◽  
Author(s):  
Ellen R. Bauer ◽  
E. Vicar Reynolds
Keyword(s):  

2016 ◽  
Vol 310 (7) ◽  
pp. R631-R639 ◽  
Author(s):  
Anthony Sclafani ◽  
Hermann Koepsell ◽  
Karen Ackroff

Recent findings suggest that the intestinal sodium-glucose transporter 1 (SGLT1) glucose transporter and sensor mediates, in part, the appetite-stimulation actions of intragastric (IG) glucose and nonmetabolizable α-methyl-d-glucopyranoside (MDG) infusions in mice. Here, we investigated the role of SGLT1 in sugar conditioning using SGLT1 knockout (KO) and C57BL/6J wild-type (WT) mice. An initial experiment revealed that both KO and WT mice maintained on a very low-carbohydrate diet display normal preferences for saccharin, which was used in the flavored conditioned stimulus (CS) solutions. In experiment 2, mice were trained to drink one flavored solution (CS+) paired with an IG MDG infusion and a different flavored solution (CS−) paired with IG water infusion. In contrast to WT mice, KO mice decreased rather than increased the intake of the CS+ during training and failed to prefer the CS+ over the CS− in a choice test. In experiment 3, the KO mice also decreased their intake of a CS+ paired with IG glucose and avoided the CS+ in a choice test, unlike WT mice, which preferred the CS+ to CS−. In experiment 4, KO mice, like WT mice preferred a glucose + saccharin solution to a saccharin solution. These findings support the involvement of SGLT1 in post-oral glucose and MDG conditioning. The results also indicate that sugar malabsorption in KO mice has inhibitory effects on sugar intake but does not block their natural preference for sweet taste.


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