Enhanced Striatal Dopamine Release During Food Stimulation in Binge Eating Disorder

Medical Department, Brookhaven National Laboratory, Upton, New York, USA.
Obesity (Impact Factor: 3.73). 02/2011; 19(8):1601-1608. DOI: 10.1038/oby.2011.27
Source: PubMed


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 methylphenidate (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 caudate and putamen in the binge eaters but not in the nonbinge eaters. Dopamine increases in the caudate were significantly correlated with the binge eating scores but not with BMI. These results identify dopamine neurotransmission in the caudate 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.

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    • "In response to food (versus non-food) images, women with BN showed greater neural activation in thè visual cortex, right dorsolateral prefrontal cortex, righi insular cortex, and precentrai gyrus, while women with AN showed greater activation in thè right dorsolateral prefrontal cortex, cerebellum, and right precuneus (Brooks et al., 2011). A recent positron emission tomographic (PET) study found dopamine dysfunction in thè caudate of obese humans with BED compared to obese humans without BED (Wang et al., 2011). Moreover, PET showed an increase of D2/D3 receptor expression in thè ventral striatum of people who recovered from AN (Frank et al., 2005). "

    Full-text · Chapter · Dec 2015
    • "Impulsivity and altered dopamine transmission are also observed in obesity and BED (Dawe & Loxton, 2004; Stice et al., 2008; Wang et al., 2011; Michaelides et al., 2012; Babbs et al., 2013; Schag et al., 2013), contributing to a widespread view that palatable energy-dense foods might be 'addictive'. Although this is a hotly debated issue (Salamone & Correa, 2013; Smith & Robbins, 2013; Ziauddeen & Fletcher, 2013), there is some consensus on the existence of 'addiction-like eating behaviour' as exemplified by bingeeating (Davis, 2013; Smith & Robbins, 2013; Ziauddeen & Fletcher, 2013; Hebebrand et al., 2014). "
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    ABSTRACT: High impulsivity, mediated through ventral striatal dopamine signaling, represents an established risk factor for substance abuse and may likewise confer vulnerability to pathological overeating. Mechanistically, the assumption is that trait impulsivity facilitates the initiation of maladaptive eating styles or choices. However, whether consumption of appetitive macronutrients themselves causes deficits in impulse control and striatal signaling, thereby contributing to cognitive changes permissive of overeating behavior, has yet to be considered. We examined the effects of chronic maintenance on restricted equicaloric, yet high-fat or high-sugar, diets (48 kcal/day; 60 kcal% fat or sucrose) on rats' performance in the 5-choice serial reaction time task (5CSRTT) indexing impulsivity and attention. Markers of dopamine signaling in the dorsal and ventral striatum, and plasma insulin and leptin levels, were also assessed. Rats maintained on the high-fat diet (HFD) were more impulsive, while the high-sugar diet (HSD) did not alter task performance. Importantly, body weight and hormone levels were similar between groups when behavioral changes were observed. Maintenance on HFD, but not HSD, reduced levels of dopamine D2 receptor (D2 R), cAMP response element-binding protein (CREB) and phospho-CREB (Ser133) proteins in the ventral, but not dorsal, striatum. D2 R expression in the ventral striatum also negatively correlated with impulsive responding independent of diet. These data indicate that chronic exposure to even limited amounts of high-fat foods may weaken impulse control and alter neural signaling in a manner associated with vulnerability to addictions-findings that have serious implications for the propagation of uncontrolled eating behavior in obesity and binge-eating disorder. This article is protected by copyright. All rights reserved.
    No preview · Article · Nov 2015 · European Journal of Neuroscience
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    • "For example, abstinent methamphetamine dependent (Stim) have blunted striatal dopamine receptor availability (Volkow et al., 2001b) associated with impulsivity (Lee et al., 2009), and individuals with AUDs have reduced ventral striatal dopamine transmission (Martinez et al., 2005) associated with alcohol craving (Heinz et al., 2004). Changes in dopamine transmission in obese subjects remains unclear with reported reductions in striatal D2 receptor binding that are associated with BMI (Wang et al., 2001) as well as no difference in underlying Dopamine (DA) capacity (Davis et al., 2009) in obese with binge eating disorder (BED) but enhanced dopamine transmission at presentation of food stimulus in BED (Wang et al., 2011). We have also recently reported enhanced premature responding in BDs at elevated risk for the development of AUD (Morris et al., 2015). "
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    ABSTRACT: The ability to wait and to weigh evidence is critical to behavioural regulation. These behaviors are known as waiting and reflection impulsivity. In Study 1, we examined the effects of methylphenidate (MPH), a dopamine and norepinephrine reuptake inhibitor, on waiting and reflection impulsivity in healthy young individuals. In Study 2, we assessed the role of learning from feedback in disorders of addiction. We used the recently developed 4-Choice Serial Reaction Time task and the Beads task. Twenty-eight healthy volunteers were tested twice in a randomized double-blind placebo controlled cross-over trial with 20mg MPH. In the second study we analyzed premature responses as a function of prior feedback in disorders of addiction. Study 1: MPH was associated with greater waiting impulsivity to a cue predicting reward along with faster responding to target onset without a generalized effect on reaction time or attention. MPH influenced reflection impulsivity based on baseline impulsivity. Study 2: more premature responses occurred after premature responses in stimulant dependent subjects. We show that MPH has dissociable effects on waiting and reflection impulsivity. Chronic stimulant exposure impairs learning from prior premature responses suggesting a failure to learn that premature responding is suboptimal. These findings provide a greater mechanistic understanding of waiting impulsivity. © The Author 2015. Published by Oxford University Press on behalf of CINP.
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