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The role of reward circuitry and food addiction in the obesity epidemic: An update

机译:奖励电路和食物成瘾在肥胖流行病中的作用:更新

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Highlights ? Altered mesolimbic dopamine circuitry has been implicated in overeating and obesity. ? In animals, food-related addiction-like behaviours are limited to binge eating models. ? In humans, food addiction is highly associated with measures of binge eating. ? Links between palatable food-related dopamine changes and addiction-like behaviour are unclear. Abstract The increasing worldwide prevalence of obesity is partially related to the ready availability of highly palatable foods which increases the incidence of hedonic, non-homeostatic feeding. The “food addiction” hypothesis postulates that exposure to these foods alters the brain’s reward circuitry, driving an addiction-like behavioural phenotype of compulsive overeating. This review highlights recent evidence that examines changes in the mesolimbic dopaminergic circuit, the primary component of the reward system, associated with exposure to highly palatable foods and obesity. The majority of obesity studies in animals have not measured addictive-like behaviours, but reports of such behaviours have been restricted to experiments using models of binge eating. Where examined, the prevalence of addiction-like behaviour in overweight and obese subjects indicates that 10–25% of the population meets the Yale Food Addiction Score criteria. There is considerable overlap in the behaviours ascribed to food addiction and binge eating disorder, and food addiction scores correlate highly with measures of binge eating. We feel that more research is required in humans to determine whether food addiction is both behaviourally and neurobiologically distinct from binge eating disorder. While the reward circuitry is clearly affected by both highly palatable foods and diet-induced obesity in a similar manner to short and long exposure to drugs of abuse, the challenge for the future is to show that these neurobiological changes are associated with addiction-like behaviour.
机译:强调 ?改变的卵泡蛋白多巴胺电路已涉及过度充分和肥胖。还在动物中,食物有关的成瘾行为仅限于狂暴的狂欢模型。还在人类中,食物成瘾与狂犬病措施高度相关。还可口与食物相关的多巴胺变化和成瘾行为之间的联系尚不清楚。摘要全球肥胖患病率的增加部分与高度可口的食物的准备好可用性部分相关,这增加了蜂窝,非稳态喂养的发生率。 “食物成瘾”假设假设暴露于这些食物的暴露改变了大脑的奖励电路,驱动了强迫暴饮暴食的成瘾性行为表型。该综述突出了最近的证据,检查了叶霉素多巴胺能电路,奖励系统的主要成分,与暴露于高度可口的食物和肥胖症相关。动物的大多数肥胖研究没有测量上瘾的行为,但这些行为的报道已被限制为使用狂欢进食的模型进行实验。在审查的情况下,超重和肥胖受试者中成瘾行为的患病率表明,10-25%的人口符合耶鲁食品成瘾评分标准。在归因于食品成瘾和狂暴饮食障碍的行为中存在相当大的重叠,并且食物成瘾分数具有高度关联,狂暴进食措施。我们觉得人类需要更多的研究,以确定食物成瘾是否行为和神经生物学均不同于狂犬病疾病。虽然奖励电路明显受到高度可口的食物和饮食诱发的肥胖的影响,但在短期和长时间地接触滥用药物的情况下,未来的挑战是表明这些神经生物学的变化与成瘾的行为有关。

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