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.
Highlights
Access to highly palatable and calorically rich foods is a major contributing factor to the increasing rates of obesity worldwide (Caballero, 2007)
The results of the present experiments show that rats fed a cafeteria diet, containing foods eaten by people, were impaired in both the value-driven guidance of food seeking responses by cues associated with palatable solutions and in the expression of sensory-specific satiety
In light of the observation that sensory-specific satiety is impaired in rats fed a cafeteria diet, and evidence that the orbitofrontal cortex (OFC) is a critical region involved in integrating an updating value-based information about reward-predictive cues (Delamater, 2007; Ostlund and Balleine, 2007; Clark et al, 2012), we suggest that that the outcome-value encoding systems are disrupted following exposure to palatable foods in cafeteria diets
Summary
Access to highly palatable and calorically rich foods is a major contributing factor to the increasing rates of obesity worldwide (Caballero, 2007). Consumption beyond basic homeostatic needs, purely based on the rewarding properties of palatable foods, is proposed to be a central contributor to the current worldwide obesity epidemic (Berthoud, 2004). A range of animal and human data demonstrates that excessive consumption of palatable food leads to changes in the sensitivity of brain reward circuitries. These reward pathways are highly conserved across species and have been associated with altered responsiveness to reward (e.g., food) in obesity. Studies have demonstrated diminished responsiveness to perform food motivated behaviors and rewarding intracranial self-stimulation in obese rats (Volkow and Wise, 2005; la Fleur et al, 2007; Pickering et al, 2009; Johnson and Kenny, 2010) and reduced sensitivity to reward (measured by ratings of motivation and pleasure derived from engaging in rewarding behaviors) in obese humans (Davis et al, 2004)
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