Exploratory study of the prevalence of food addiction and its relationship with executive functioning, depression, and reinforcement sensitivity in a sample of Mexican adults.

Introduction: The study of food addiction (FA) has become relevant due to its high prevalence, the negative impact on quality of life, and its association with neuropsychological and psychiatric symptoms. Several studies have provided scientific support for these associations, however, the results are contradictory. Additionally, studies have unsuccessfully elucidated the true nature of the failures in executive functioning in people with FA symptomatology, particularly when it comes to executive deficits.

Stimulation of melanocortin-3 receptors accelerates the satiation process and increases the α-MSH expression in high-fat diet-fed rats.

The knowledge about the role of MC3 receptors (MC3r) in the regulation of feeding behavior is limited. The present study was conducted to determine whether MC3r mediates the hypophagic effects of the melanocortins under conditions of positive energy balance. Male Wistar rats were fed with a high-fat diet (HFD) for 15 days and on day 16 the animals received an intracerebroventricular injection of the following treatments: Vehicle, D-Trp8-γ-melanocyte-stimulating hormone (MSH; MC3r agonist), SHU9119 (MC3r/MC4r antagonist), or D-Trp8-γ-MSH+SHU9119.

CB1/5-HT/GABA interactions and food intake regulation.

Despite historically the serotonergic, GABAergic, and cannabinoid systems have been shown to play a crucial role in the central regulation of eating behavior, interest in the study of the interactions of these neurotransmission systems has only now been investigated. Current evidence suggests that serotonin may influence normal and pathological eating behavior in significantly more complex ways than was initially thought. This knowledge has opened the possibility of exploring the potential clinical utility of new therapeutic strategies more effective and safer than the current approaches to treat pathological eating behavior.

CB1 receptors in the paraventricular nucleus of the hypothalamus modulate the release of 5-HT and GABA to stimulate food intake in rats.

Endocannabinoids and their receptors not only contribute to the control of natural processes of appetite regulation and energy balance but also have an important role in the pathogenesis of obesity. CB1 receptors (CB1R) are expressed in several hypothalamic nuclei, including the paraventricular nucleus (PVN), where induce potent orexigenic responses. Activation of CB1R in the PVN induces hyperphagia by modulating directly or indirectly orexigenic and anorexigenic signals; however, interaction among these mediators has not been clearly defined.

Stimulation of dopamine D4 receptors in the paraventricular nucleus of the hypothalamus of male rats induces hyperphagia: involvement of glutamate.

Obesity is a serious worldwide health problem, affecting 20-40% of the population in several countries. According to animal models, obesity is related to changes in the expression of proteins that control energy homeostasis and in neurotransmission associated to regulation of food intake. For example, it has been reported that diet-induced obesity produces overexpression of dopamine D4 receptor (D4R) mRNA in the ventromedial hypothalamic nucleus (VMH) of mice.

The effects of 5-HT1A and 5-HT2C receptor agonists on behavioral satiety sequence in rats.

The present study examined the effects of 5-HT1A and 5-HT2C receptor agonists on behavioral satiety sequence (BSS) in rats. The 5-HT1A receptor agonist, 8-OH-DPAT (0.5 microg), and the 5-HT2C receptor agonist, Ro-60-0175 (3.

Role of 5-HT1A and 5-HT1B receptors in the hypophagic effect of 5-HT on the structure of feeding behavior.

Background: Feeding behavior is deeply affected by serotonergic neurotransmission. This regulatory activity is mediated mainly by specific 5-HT1/2 receptors, and the paraventricular nucleus (PVN) plays a key role in this phenomena. In order to reveal the involvement of 5-HT1A and 5-HT1B receptors in the paraventricular nucleus of the hypothalamus (PVN) on serotonin-induced hypophagia, we examined the effects of intra-PVN injections of serotonin in WAY 100635 or SB 216641-pretreated rats on the structure of feeding behavior.