12/18/2023 0 Comments Hedonic motivesThese hormones, including cholecystokinin (CCK), peptide YY (PYY), and glucagon-like peptide 1 (GLP-1), suppress homeostatic hunger and promote satiation and satiety mainly through hindbrain circuits, thus governing meal-by-meal eating behavior. Several gastrointestinal endocrine cells produce and secrete satiety hormones in response to food consumption and digestion. Importantly, anticipatory effects to food are brain mediated, while changes in peripheral hormones are a related consequence. Therefore, understanding the physiological and pathophysiological mechanisms underlying the hedonic hunger may help to counteract obesity.Īnimal data support the view that distinguishable although overlapping neural and peripheral pathways, involving several appetite-regulating substances, drive homeostatic- and hedonic-based eating ( 4, 5). Indeed, mismatch between the hedonic value attributed to food and energy needs is characteristic of eating disorders, including (morbid) obesity. An emerging hypothesis concerns the role of the brain's reward system that responds to the stimulus provided by rewarding and palatable ‘obesogenic’ foods and appears to override the homeostatic signals for body weight control ( 3). ![]() Thus, both the palatability and availability of foods in the Western diet play a major role in the development of this (dramatically widespread) disease ( 2). ![]() ![]() Reportedly, obesity reflects an energy imbalance in which genetically susceptible individuals become increasingly vulnerable to an ‘obesogenic’ environment. This phenomenon has been defined as ‘hedonic hunger’ in contraposition with ‘homeostatic hunger’, which is essentially triggered by energy deprivation ( 1). In fact, food intake is motivated not only by the need to restore energy homeostasis palatable, rewarding high-fat and/or sugar foods such as chocolate can motivate eating despite a state of satiety and positive energy balance.
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