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. 2014 Aug 27:5:852.
doi: 10.3389/fpsyg.2014.00852. eCollection 2014.

Cafeteria diet impairs expression of sensory-specific satiety and stimulus-outcome learning

Affiliations

Cafeteria diet impairs expression of sensory-specific satiety and stimulus-outcome learning

Amy C Reichelt et al. Front Psychol. .

Abstract

A range of animal and human data demonstrates that excessive consumption of palatable food leads to neuroadaptive responses in brain circuits underlying reward. Unrestrained consumption of palatable food has been shown to increase the reinforcing value of food and weaken inhibitory control; however, whether it impacts upon the sensory representations of palatable solutions has not been formally tested. These experiments sought to determine whether exposure to a cafeteria diet consisting of palatable high fat foods impacts upon the ability of rats to learn about food-associated cues and the sensory properties of ingested foods. We found that rats fed a cafeteria diet for 2 weeks were impaired in the control of Pavlovian responding in accordance to the incentive value of palatable outcomes associated with auditory cues following devaluation by sensory-specific satiety. Sensory-specific satiety is one mechanism by which a diet containing different foods increases ingestion relative to one lacking variety. Hence, choosing to consume greater quantities of a range of foods may contribute to the current prevalence of obesity. We observed that rats fed a cafeteria diet for 2 weeks showed impaired sensory-specific satiety following consumption of a high calorie solution. The deficit in expression of sensory-specific satiety was also present 1 week following the withdrawal of cafeteria foods. Thus, exposure to obesogenic diets may impact upon neurocircuitry involved in motivated control of behavior.

Keywords: Pavlovian conditioning; devaluation; incentive value; obesity; sensory-specific satiety.

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Figures

FIGURE 1
FIGURE 1
Design and timeline of the studies. (A) Cue-outcome devaluation and (B) Sensory-specific satiety, indicating outcomes [cherry sucrose, grape maltodextrin, or no reward (Ø)].
FIGURE 2
FIGURE 2
(A) Body weight of cafeteria (N = 16) and chow (N = 16) diet rats. (B) Total energy intake over 24 h (kJ/rat). (C) Macronutrient intake over 24 h (protein, carbohydrate, and fat) as energy (kJ/rat). Data presented as mean (±SEM). *p < 0.05, ***p ≤ 0.001 compared to chow, Bonferroni corrected.
FIGURE 3
FIGURE 3
(A) Magazine responding in the final training session; (B) Magazine responding (Mean CS1-3) at test and (C) Mean magazine responding at test across all CSfor chow diet rats (N = 14) and cafeteria diet rats (N = 15). Data presented as mean (±SEM). *p < 0.05, **p < 0.01 Bonferroni corrected.
FIGURE 4
FIGURE 4
Consumption of sample solutions during (A) Familiarization to the two solutions, (B) Pre-exposure to the solutions prior to test, (C) Sensory-specific satiety test indicating the mean volume consumed of the pre-exposed and non-pre-exposed solutions during two bottle choice testing by chow (N = 16) and cafeteria (N = 16) diet fed rats. Data presented as mean (±SEM). **p < 0.01, ***p < 0.001. Bonferroni corrected.
FIGURE 5
FIGURE 5
Two bottle choice test of sensory-specific satiety following pre-exposure to palatable solutions in rats 1 week after withdrawal of the cafeteria diet (N = 12) and chow fed control rats (N = 12). Data presented as mean (±SEM). ***p < 0.001.Bonferroni corrected.

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