Insula to ventral striatal projections mediate compulsive eating produced by intermittent access to palatable food

Compulsive eating characterizes many binge-related eating disorders, yet its neurobiological basis is poorly understood. The insular cortex subserves visceral-emotional functions, including taste processing, and is implicated in drug craving and relapse. Here, via optoinhibition, we implicate projections from the anterior insular cortex to the nucleus accumbens as modulating highly compulsive-like food self-administration behaviors that result from intermittent access to a palatable, high-sucrose diet. We identified compulsive-like eating behavior in female rats through progressive ratio schedule self-administration and punishment-resistant responding, food reward tolerance and escalation of intake through 24-h energy intake and fixed-ratio operant self-administration sessions, and withdrawal-like irritability through the bottle brush test. We also identified an endocrine profile of heightened GLP-1 and PP but lower ghrelin that differentiated rats with the most compulsive-like eating behavior. Measures of compulsive eating severity also directly correlated to leptin, body weight and adiposity. Collectively, this novel model of compulsive-like eating symptoms demonstrates adaptations in insula-ventral striatal circuitry and metabolic regulatory hormones that warrant further study

Rimonabant Precipitates Anxiety in Rats Withdrawn from Palatable Food: Role of the Central Amygdala

The anti-obesity medication rimonabant, an antagonist of cannabinoid type-1 (CB1) receptor, was withdrawn from the market because of adverse psychiatric side effects, including a negative affective state. We investigated whether rimonabant precipitates a negative emotional state in rats withdrawn from palatable food cycling. The effects of systemic administration of rimonabant on anxiety-like behavior, food intake, body weight, and adrenocortical activation were assessed in female rats during withdrawal from chronic palatable diet cycling. The levels of the endocannabinoids, anandamide and 2-arachidonoylglycerol (2-AG), and the CB1 receptor mRNA and the protein in the central nucleus of the amygdala (CeA) were also investigated. Finally, the effects of microinfusion of rimonabant in the CeA on anxiety-like behavior, and food intake were assessed. Systemic administration of rimonabant precipitated anxiety-like behavior and anorexia of the regular chow diet in rats withdrawn from palatable diet cycling, independently from the degree of adrenocortical activation. These behavioral observations were accompanied by increased 2-AG, CB1 receptor mRNA, and protein levels selectively in the CeA. Finally, rimonabant, microinfused directly into the CeA, precipitated anxiety-like behavior and anorexia. Our data show that (i) the 2-AG-CB1 receptor system within the CeA is recruited during abstinence from palatable diet cycling as a compensatory mechanism to dampen anxiety, and (ii) rimonabant precipitates a negative emotional state by blocking the beneficial heightened 2-AG-CB1 receptor signaling in this brain area. These findings help elucidate the link between compulsive eating and anxiety, and it will be valuable to develop better pharmacological treatments for eating disorders and obesity

Preclinical models of stress and environmental influences on binge eating

Preclinical models cannot explain all of the complex internal and external factors that influence eating behaviors in humans. Still, they represent an essential tool to investigate the underlying neuro- and psychobiology implicated in disorders that are associated with binge eating. Several environmental conditions induce aberrant feeding behavior on calorie-dense food in animal models of binge eating. Various kinds of stress (acute or chronic), the combination of repeated cycles of food restriction and refeeding plus stress, food deprivation, and limited access to palatable food have been used to elicit binge-like eating episodes to model human behaviors. Animal studies have revealed the involvement of different neurotransmitter pathways, especially dopamine, opioids, CRF, serotonin, orexin, and GABAergic systems in binge-like eating. They may aid in the ultimate goal of identifying novel, safe, and effective therapeutic targets

Turkish version of the Yale Food Addiction Scale

Background Yale Food Addiction Scale (YFAS) was established to identify individuals exhibiting signs of addiction towards certain types of food. This study aimed to develop a Turkish version of the Yale Food Addiction Scale and test its psychometric properties. Methods The backward translation techniques were used to develop Turkish versions of the YFAS, and its reproducibility was assessed. Turkish version of the YFAS was administered to a total of 1033 participants (439 men and 594 women), aged 19–65 years. Exploratory factor analysis and confirmatory factor analysis were used to examine the factorial structure of the tool. Construct validity was assessed by principal component factor analysis with varimax rotation. Reliabilities were estimated with Cronbach’s alpha coefficient. The criterion-related validity was tested by the administration of Eating Attitude Test-26 (EAT-26) to all participants. Results The primary factor loadings for seven items were ranged between 0.45 and 0.79, and no items cross-loaded onto other factors. The fit indices showed that eight items of the YFAS were a good representation of the item responses and each item loaded significantly on the specified factor (p < 0.001 for each). YFAS subscales had a high internal consistency and test–retest reliability. The criterion-related validity of the tool showed a positive relationship with scales of the EAT-26. Conclusion Current study suggested that the Turkish version of the YFAS is a reliable, valid, and useful tool for assessing the signs of food addiction in a non-clinical sample.PubMedWoSScopu