Interaction of satiety and reward response to food stimulation.
Obesity is among the most pressing health issues affecting developed countries. The etiology of obesity remains unclear despite its associated health risks. We propose a framework for obesity modeled upon overeating as a substance dependence disorder arising from a combination of abnormal cognitive and neuroendocrine processes. While significant work in both of these fields has investigated the body's regulation of satiety signals, fewer studies have focused upon the mechanisms by which these two seemingly disparate systems interact. Although emotional states have been shown to mediate reward processing, the implications for hunger mediating reward have not previously been addressed. We review the interaction between central satiety signals and reward responses to food stimuli and discuss the implications of this research for understanding the causes of obesity.
James
G Andrew
GA
University of Florida College of Medicine, Department of Psychiatry, Gainesville, FL 32610-0256, USA.
Gold
Mark S
MS
Liu
Yijun
Y
D000339:Affect / Q000502:physiology; D001069:Appetite Regulation / Q000502:physiology; D001921:Brain / Q000378:metabolism / Q000503:physiopathology; D003071:Cognition; D003937:Diagnosis, Differential; D002149:Energy Intake / Q000502:physiology*; D005215:Fasting; D005502:Food; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007003:Hypoglycemia / Q000503:physiopathology; D008279:Magnetic Resonance Imaging; D009765:Obesity / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology*; D011218:Prader-Willi Syndrome / Q000503:physiopathology; D011582:Psychological Theory; D012201:Reward; D012528:Satiety Response / Q000502:physiology*; D019966:Substance-Related Disorders / Q000175:diagnosis*
D005947:Glucose