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Central, peripheral, and contextual regulation of food intake


Near-unlimited access to energy-dense foods high in fat and sugar is widely viewed as a major contributing factor to the obesity epidemic of modern industrialized nations. Excessive consumption of these highly palatable foods, however, may have consequences on physiological and psychological function that extend beyond gains in body weight. Like drugs of abuse, palatable foods acquire enhanced incentive salience with repeated exposure, reflecting increased motivation to obtain and consume them. Whether palatable foods, similar to drugs of abuse, can also produce a withdrawal-like syndrome upon cessation of access remains unclear. This dissertation describes a model of rapid, excessive 'binge-like' intake of a highly palatable sweet fat diet in rats, investigates whether evidence of a withdrawal-like syndrome or impaired reward function is apparent during the abstinent period between binges, and explores the contribution of cannabinoid type 1(CB1) receptor mediated signals in regulating binge-like behavior. Results indicated that limited daily access to the sweet fat diet induced robust binge-like behavior in the absence of negative emotional symptoms of anxiety-like behavior or impaired reward function upon withdrawal. However, rats with a history of binge-like palatable food intake did show evidence of enhanced reactivity to binge- related cues. A binge "prime" consisting of a minimal dose of the sweet fat diet and contextual cues associated with the binge increased locomotor indices of activity and elevated intracranial self-stimulation thresholds. This suggests that the primary factors motivating continued binge-like intake are the hedonic value of the food and the appetitive drive associated with binge cues rather than an attempt to compensate for a negative state of withdrawal. Using a novel CB1 receptor inverse agonist, the hypothesis that central and peripheral cannabinoid receptors contribute independently to regulation of binge- like food intake was also tested. Peripheral CB1 blockade reduced ad libitum intake of both less palatable chow and the palatable diet, but joint blockade of central and peripheral receptors was required to suppress binge-like intake. This suggests that central cannabinoid circuitry is preferentially recruited when incentive to consume a palatable food is enhanced by limited access

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