Research Article: The Influence of Palatable Diets in Reward System Activation: A Mini Review

Date Published: March 20, 2016

Publisher: Hindawi Publishing Corporation

Author(s): Isabel Cristina de Macedo, Joice Soares de Freitas, Iraci Lucena da Silva Torres.


The changes in eating patterns that have occurred in recent decades are an important cause of obesity. Food intake and energy expenditure are controlled by a complex neural system involving the hypothalamic centers and peripheral satiety system (gastrointestinal and pancreatic hormones). Highly palatable and caloric food disrupts appetite regulation; however, palatable foods induce pleasure and reward. The cafeteria diet is such a palatable diet and has been shown consistently to increase body weight and induce hyperplasia in animal obesity models. Moreover, palatable high-fat foods (such as those of the cafeteria diet) can induce addiction-like deficits in brain reward function and are considered to be an important source of motivation that might drive overeating and contribute to the development of obesity. The mechanism of neural adaptation triggered by palatable foods is similar to those that have been reported for nondrug addictions and long-term drug use. Thus, this review attempts to describe the potential mechanisms that might lead to highly palatable diets, such as the cafeteria diet, triggering addiction, or compulsion through the reward system.

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Currently, an important cause of obesity has been observed to be related to changes in eating patterns that have occurred in recent decades [1]. The daily consumption associated with so-called Western diets consists of highly palatable and caloric food [2], and such diets have become a habit that has led many individuals to develop obesity [3]. Recent studies using the cafeteria diet as an experimental model of obesity with or without associated chronic stress have shown that animals exposed to this diet became obese and exhibit important changes in lipid profiles, endocrine appetite markers, and the development of hyperphagia [4, 5].

Food control is a complex mechanism that involves the appetite, motivation, and energy demands of the organism and these aspects can be modified by food availability and exposure. The central nervous system detects a wide variety of peripheral neural and humoral markers, and this complex neural network receives endocrine and hormonal inputs. Hormones, such as leptin, insulin, pancreatic polypeptide (PP), amylin, ghrelin, cholecystokinin, glucagon-like peptide (GLP-1), and oxyntomodulin, coordinate food intake through signaling and modulation in orexigenic and anorexigenic neurons (for review see [9]). These markers reflect gastrointestinal functions and energy needs, including taste, which is a central factor in decision-making related to feeding behavior, and the olfaction. Both functions are capable of discriminating features such as odor, texture, and temperature and participating in the choice of food to be ingested [10]. The homeostasis regulation and maintenance of stable body weight depend on the integration of these signals and on the ability to respond appropriately through modulation of energy expenditure and food intake [11]. Hypothalamic centers control food intake and weight gain and are part of a complex of neuroregulatory interactions that include the peripheral satiety system (gastrointestinal and pancreatic hormones) and a large-scale central neural network [12]. The importance of the hypothalamus in energy homeostasis was first suggested by classic lesioning experiments performed rodents, and subsequent studies suggested the roles of hypothalamic nuclei, such as the arcuate nucleus (ARC), paraventricular nucleus (PVN), ventromedial nucleus (VMN), dorsomedial region (DMV), and lateral hypothalamic area (LHA), in energy homeostasis [13]. The blood-brain barrier (BBB) adjacent to the ARC region serves as the interface of the peripheral metabolic signals and the brain. While the DMV area is the region of satiety, the LH nuclei are the main controllers of feeding responses [14]. Damage to the hypothalamus, particularly the lateral and dorsomedial hypothalamus, disrupts feeding behavior [15]. Food intake and energy metabolism are regulated by a complex interaction between orexigenic and anorexigenic neuropeptides in the ARC of the hypothalamus and peripheral tissues. Neuropeptide Y (NPY) and agouti-related protein (AgRP) are coexpressed in neurons of the ARC and are potent orexigenic peptides. Additionally, the α-melanocyte-stimulating hormone (α-MSH) and cocaine- and amphetamine-regulated transcript (CART) peptide are potent anorexigens [16]. The hypothalamic nucleus receives inputs of several peripheral hormones including leptin; for example, the arcuate nucleus of the hypothalamus and the area postrema of the nucleus tractus solitarius express leptin receptors and are important regions of appetite control and food ingestion. Leptin is a hormone that is synthesized and released by adipose tissue and acts as food control in the ARC of the hypothalamus. This hormone stimulates neurons to secrete proopiomelanocortin (POMC), which is a precursor protein of α-MSH that also stimulates POMC neurons to secrete CART. Leptin also inhibits AgRP/NPY neurons, which coexpress the orexigenic neuropeptides AgRP and NPY, and antagonizes α-MSH. The combined effect of the actions of leptin suppresses appetite and contributes to the maintenance of energy homeostasis (for review see [17]). Another important hormone that is related to food control is ghrelin. This hormone is produced by the stomach, hypothalamus (ARC and infundibular nucleus), and pituitary gland. After being released into the blood stream, ghrelin reaches the ARC and activates NPY and AgRP neurons, which leads to increased food intake [18]. In addition to acting on dietary control, both leptin and ghrelin are involved in the reward system [17, 18]. Leptin receptors are also found in the mesolimbic pathway in the reward-associated ventral tegmental area (VTA) and the substantia nigra [19]. Thus, leptin influences the hedonic aspects of feeding and interacts with the mesolimbic-dopaminergic system, which is known to regulate arousal, mood, and reward (for review see [17]), while ghrelin stimulates dopamine neurons in the ventral tegmental area (VTA) and promotes dopamine turnover in the nucleus accumbens of the ventral striatum, which is part of the major central reward pathway (for review see [18]). Accordingly the balance between food control centers and peripheral signals determines appetite and energy expenditure and influences the reward system.

Palatable foods with high fat and sugar contents are associated with increased food intake [7, 20]. Palatable foods alter the behavior of experimental animals. In a study of obese rats with histories of extended access to palatable food, the rats were found to continue to eat palatable food even in the presence of a noxious light cue that predicted the delivery of an aversive foot shock [7]. Moreover, mice that have previously had access to a palatable high-fat diet spend more time in an aversive environment to obtain the palatable food than do mice with no prior experience of the diet [21].

Obesity is a global pandemic and major health burden with the associated risk factors of cardiovascular disease and diabetes mellitus. The current dietary patterns predominantly include high calorie foods that are high in fat and sugar as exemplified by the cafeteria diet, which has been used as an animal model. Such diets unleash pleasure and lead to drastic increases in food intake. These foods lead to disruptions of several signaling pathways that are related to food control, including activation of the reward system. Thus, palatable foods lead to addiction through mechanisms that are similar to those of drugs of abuse. This scenario increases the level of difficulty related to the planning and development of new pharmacological strategies for obese patients.