A Perspective on Candidate Neural Underpinnings of Binge Eating Disorder: Reward and Homeostatic Systems

被引:7
|
作者
Romei, Amelia [1 ,2 ]
Voigt, Katharina [1 ,2 ]
Vardejo-Garcia, Antonio [1 ,2 ]
机构
[1] Monash Univ, Sch Psychol Sci, Clayton, Vic 3800, Australia
[2] Monash Univ, Turner Inst Brain & Mental Hlth, Clayton, Vic 3800, Australia
关键词
Binge eating disorder; resting-state functional magnetic resonance imaging; functional magnetic resonance imaging; reward; hunger; feeding behaviour; STATE FUNCTIONAL CONNECTIVITY; HUMAN ORBITOFRONTAL CORTEX; RISK-FACTORS; HUMAN BRAIN; FOOD; ACTIVATION; WOMEN; RESPONSES; SATIETY; HUNGER;
D O I
10.2174/1381612826666200309152321
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
People with Binge Eating Disorder (BED) exhibit heightened sensitivity to rewarding stimuli and elevated activity in reward-related brain regions, including the orbitofrontal cortex (OFC), ventral striatum (VS) and insula, during food-cue exposure. BED has also been associated with altered patterns of functional connectivity during resting-state. Investigating neural connectivity in the absence of task stimuli provides knowledge about baseline communication patterns that may influence the behavioural and cognitive manifestation of BED. Elevated resting-state functional connectivity (rsFC) between reward-related brain regions may contribute to uncontrolled eating bouts observed in BED, through heightened food-cue sensitivity and food-craving. The impact of homeostatic state on rsFC of the reward system has not yet been investigated in people with BED. Homeostatic dysfunction is a key driver of excessive food consumption in obesity, whereby rsFC between reward-related brain regions does not attenuate during satiety. Future studies should investigate BED related differences in rsFC within the reward system during hunger and satiety, in order to determine whether individuals with BED display an abnormal neural response to changes in homeostatic state. This knowledge would further enhance current understandings of the mechanisms contributing to BED, potentially implicating both reward and homeostatic dysfunctions as drivers of BED.
引用
收藏
页码:2327 / 2333
页数:7
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