Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats
Paul M Johnson,Paul J. Kenny +1 more
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TLDR
Overconsumption of palatable food triggers addiction-like neuroadaptive responses in brain reward circuits and drives the development of compulsive eating, demonstrating that common hedonic mechanisms may underlie obesity and drug addiction.Abstract:
We found that development of obesity was coupled with emergence of a progressively worsening deficit in neural reward responses. Similar changes in reward homeostasis induced by cocaine or heroin are considered to be crucial in triggering the transition from casual to compulsive drug-taking. Accordingly, we detected compulsive-like feeding behavior in obese but not lean rats, measured as palatable food consumption that was resistant to disruption by an aversive conditioned stimulus. Striatal dopamine D2 receptors (D2Rs) were downregulated in obese rats, as has been reported in humans addicted to drugs. Moreover, lentivirus-mediated knockdown of striatal D2Rs rapidly accelerated the development of addiction-like reward deficits and the onset of compulsive-like food seeking in rats with extended access to palatable high-fat food. These data demonstrate that overconsumption of palatable food triggers addiction-like neuroadaptive responses in brain reward circuits and drives the development of compulsive eating. Common hedonic mechanisms may therefore underlie obesity and drug addiction.read more
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Reward, dopamine and the control of food intake: implications for obesity
TL;DR: Imaging studies show that obese subjects might have impairments in dopaminergic pathways that regulate neuronal systems associated with reward sensitivity, conditioning and control, and it is postulated that this could also be a mechanism by which overeating and the resultant resistance to homoeostatic signals impairs the function of circuits involved in reward sensitivity.
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Preliminary validation of the Yale Food Addiction Scale
TL;DR: The Yale Food Addiction Scale (YFAS) is a sound tool for identifying eating patterns that are similar to behaviors seen in classic areas of addiction, and predicted binge-eating behavior above and beyond existing measures of eating pathology, demonstrating incremental validity.
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The tempted brain eats: Pleasure and desire circuits in obesity and eating disorders
TL;DR: This work assesses brain mechanisms known to generate "liking" and "wanting" for foods and evaluates their interaction with regulatory mechanisms of hunger and satiety, relevant to clinical issues.
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Patchy progress on obesity prevention: emerging examples, entrenched barriers, and new thinking
Christina A. Roberto,Boyd Swinburn,Corinna Hawkes,Terry T.-K. Huang,Terry T.-K. Huang,Sergio A. Costa,Sergio A. Costa,Marice Ashe,Lindsey Zwicker,John Cawley,Kelly D. Brownell +10 more
TL;DR: A reframing of obesity is proposed that emphasises the reciprocal nature of the interaction between the environment and the individual, and concludes that people bear some personal responsibility for their health, but environmental factors can readily support or undermine the ability of people to act in their own self-interest.
References
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TL;DR: Dopamine modulates motivation and reward circuits and hence dopamine deficiency in obese individuals may perpetuate pathological eating as a means to compensate for decreased activation of these circuits.
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Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake
TL;DR: The evidence supports the hypothesis that under certain circumstances rats can become sugar dependent and may translate to some human conditions as suggested by the literature on eating disorders and obesity.