Article

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

ABSTRACT

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). "

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    • "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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    • "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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