***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Binge eating is a core clinical feature of bulimia nervosa ( BN ) . Enhanced reinforcing value of food may play a role in this behavioral disturbance , but a systematic behavioral assessment of objective measures of the rewarding value of binge eating is lacking . The purpose of this study was to quantify the reinforcing value of food in BN patients as compared with normal controls . A progressive ratio ( PR ) computerized work task was completed under binge and non-binge instruction . The task consisted of 12 trials . The first trial required 50 keyboard taps to earn one portion of yogurt shake , and subsequent trials required progressive work increments of 200 taps for each additional portion . Completion of all 12 trials required 13,800 taps to earn 2100ml of shake . The breakpoint , defined as the largest ratio completed before a participant stopped working , was the measure of reinforcing efficacy . Ten patients and 10 controls completed the experiment . Under binge instruction , patients completed more trials and taps , and had a higher breakpoint than controls . The non-binge instruction yielded opposite findings ; compared to controls , patients completed fewer trials and taps , and had a lower breakpoint . These results support the feasibility and potential utility of a PR task to quantify the reinforcing value of food in patients with BN Subjects with binge eating disorder ( BED ) regularly consume large amounts of food in short time periods . The neurobiology of BED is poorly understood . Brain dopamine , which regulates motivation for food intake , is likely to be involved . We assessed the involvement of brain dopamine in the motivation for food consumption in binge eaters . Positron emission tomography ( PET ) scans with [(11)C]raclopride were done in 10 obese BED and 8 obese subjects without BED .  Changes in extracellular dopamine in the striatum in response to food stimulation in food-deprived subjects were evaluated after placebo and after oral methylpheni date ( MPH ) , a drug that blocks the dopamine reuptake transporter and thus amplifies dopamine signals . Neither the neutral stimuli ( with or without MPH ) nor the food stimuli when given with placebo increased extracellular dopamine . The food stimuli when given with MPH  significantly increased dopamine in the cau date and putamen in the binge eaters but not in the nonbinge eaters . Dopamine increases in the cau date were significantly correlated with the binge eating scores but not with BMI . These results identify dopamine neurotransmission in the cau date as being of relevance to the neurobiology of BED . The lack of correlation between BMI and dopamine changes suggests that dopamine release per se does not predict BMI within a group of obese individuals but that it predicts binge eating BACKGROUND Several lines of evidence support the possibility that disturbances of dopamine ( DA ) function could contribute to alterations of weight , feeding , motor activity , and reward in anorexia nervosa ( AN ) . METHODS To assess possibly trait-related disturbances but avoid confounding effects of malnutrition , 10 women who were recovered from AN ( REC AN ) were compared with 12 healthy control women ( CW ) .  Positron emission tomography with [(11)C]raclopride was used to assess DA D2/D3 receptor binding . RESULTS The women who were recovered from AN had significantly higher [(11)C]raclopride binding potential in the antero-ventral striatum than CW . For REC AN , [(11)C]raclopride binding potential was positively related to harm avoidance in the dorsal cau date and dorsal putamen . CONCLUSIONS These data lend support for the possibility that decreased intrasynaptic DA concentration or increased D2/D3 receptor density or affinity is associated with AN and might contribute to the characteristic harm avoidance or increased physical activity found in AN . Most intriguing is the possibility that individuals with AN might have a DA related disturbance of reward mechanisms contributing to altered hedonics of feeding behavior and their ascetic , anhedonic temperament 
    Output:
    
The 5-HT transporter ( 5-HTT ) binding was increased or diminished in different specific cortical areas and in relation to Eating Disorder ( ED ) subtypes .
Some evidence s of blunted Dopamine ( DA ) release in the putamen in BN patients suggest that their DA function might be impaired as in addictive behaviours .
Studies estimating the regional Cerebral Blood Flow ( rCBF ) with SPECT demonstrated that temporal areas seem to play a key role in ED corroborating the hypothesis of a cingulate-temporal cortical dysfunction in AN .
In addition , alterations of both parietal and prefrontal cortex provide a possible common neural substrate in AN .
Studies included in this review are heterogeneous preventing robust conclusions , however , our findings add knowledge on some of the neurotransmitters involved in ED