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About the Authors:
Gene-Jack Wang
* E-mail: [email protected]
Affiliation: Laboratory of Neuroimaging, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland, United States of America
Dardo Tomasi
Affiliation: Laboratory of Neuroimaging, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland, United States of America
Antonio Convit
Affiliations Department of Psychiatry, New York University, New York, New York, United States of America, Nathan Kline Institute for Psychiatric Research, Orangeburg, New York, United States of America
Jean Logan
Affiliation: Department of Psychiatry, New York University, New York, New York, United States of America
Christopher T. Wong
Affiliation: Laboratory of Neuroimaging, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland, United States of America
Elena Shumay
Affiliation: Laboratory of Neuroimaging, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland, United States of America
Joanna S. Fowler
Affiliation: Biosciences Department, Brookhaven National Laboratory, Upton, New York, United States of America
Nora D. Volkow
Affiliation: Laboratory of Neuroimaging, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland, United States of America
Introduction
Brain dopamine (DA) modulates eating behaviors through its modulation of reward and incentive salience [1]. Activation of DA in the nucleus accumbens (NAc) occurs with exposure to novel food rewards but with repeated exposures DA increases instead shift to the cues that predict the food reward [2]. The mesolimbic DA system is critical for reinforcing food palatability and highly palatable foods increase DA in NAc [3], whereas DA antagonists attenuate the hedonic value of sucrose [4]. DA also mediates the rewarding effects of food that are driven by energy content [5]. Rodent studies revealed intragastric administration of glucose increased DA in NAc [6], which was an effect dependent on glucose utilization, since administration of an anti-metabolic glucose analog lowered DA. This indicates that DA neurons respond to the energetic value of nutrients independent of taste and implicates postingestive factors in calorie related DA increases in NAc. Moreover in humans neuroimaging studies have shown that sucrose solution but not a non-caloric sweet solution activates the midbrain, which is where DA neurons are located [7]. DA neurons are also activated by visual, auditory and somatosensory stimuli that predict food reward [8]. Excessive food consumption can lead to obesity, which, in turn triggers metabolic adaptations that further perpetuate excessive food consumption....