6533b838fe1ef96bd12a448b
RESEARCH PRODUCT
Integration of Peripheral Adiposity Signals and Psychological Controls of Appetite
Alfred J. SipolsNicole M. SandersAmy M. NaleidDianne Figlewicz Lattemannsubject
Efferentmedia_common.quotation_subjectLeptinCentral nervous systemAppetiteStimulus (physiology)Neurochemicalmedicine.anatomical_structureNegative feedbackmedicineBrain stimulation rewardPsychologyNeurosciencemedia_commondescription
Publisher Summary This chapter presents an overview of the major anatomical and neurochemical participants in brain reward circuitry. It also elaborates the evidence available to date that supports the hypothesis that energy regulatory signals can modulate food reward. Psychological modulation of feeding involves taste hedonics and preferences, and the rewarding aspects of food. The brain circuitries implicated in stimulus reward, and in the regulation of energy balance, have traditionally been considered as separate. However, more recently, accumulated evidence suggests that there is both anatomical and functional crosstalk between these sets of central nervous system (CNS) circuitry. Adding to the potential crosstalk is evidence for modulation by the peripheral adiposity signals insulin and leptin. The chapter further discusses that energy regulatory circuitry is intricately linked with reward circuitry. Energy regulatory circuitry is part of a negative feedback loop, which includes the generation of peripheral signals that reflect body adipose stores, and these signals act primarily at the medial hypothalamus to regulate the efferent components of this feedback loop, specifically food intake and energy balance. The reward circuitry ultimately should not be viewed as functionally separate from energy regulatory circuitry, but as part of the loop as suggested by the CNS anatomy. Inputs from reward circuitry are critical component of the total CNS network that regulates food intake. These findings open the possibility for more extensive interaction between the two circuitries mediated by endogenous CNS neurotransmitters.
year | journal | country | edition | language |
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2007-01-01 |