scholarly journals Oleoylethanolamide decreases frustration stress-induced binge-like eating in female rats: a novel potential treatment for binge eating disorder

2020 ◽  
Vol 45 (11) ◽  
pp. 1931-1941 ◽  
Author(s):  
Adele Romano ◽  
Maria Vittoria Micioni Di Bonaventura ◽  
Cristina Anna Gallelli ◽  
Justyna Barbara Koczwara ◽  
Dorien Smeets ◽  
...  

Abstract Binge eating disorder (BED) is the most frequent eating disorder, for which current pharmacotherapies show poor response rates and safety concerns, thus highlighting the need for novel treatment options. The lipid-derived messenger oleoylethanolamide (OEA) acts as a satiety signal inhibiting food intake through the involvement of central noradrenergic and oxytocinergic neurons. We investigated the anti-binge effects of OEA in a rat model of binge-like eating, in which, after cycles of intermittent food restrictions/refeeding and palatable food consumptions, female rats show a binge-like intake of palatable food, following a 15-min exposure to their sight and smell (“frustration stress”). Systemically administered OEA dose-dependently (2.5, 5, and 10 mg kg−1) prevented binge-like eating. This behavioral effect was associated with a decreased activation (measured by mapping the expression of c-fos, an early gene widely used as a marker of cellular activation) of brain areas responding to stress (such as the nucleus accumbens and amygdala) and to a stimulation of areas involved in the control of food intake, such as the VTA and the PVN. These effects were paralleled, also, to the modulation of monoamine transmission in key brain areas involved in both homeostatic and hedonic control of eating. In particular, a decreased dopaminergic response to stress was observed by measuring dopamine extracellular concentrations in microdialysates from the nucleus accumbens shell, whereas an increased serotonergic and noradrenergic tone was detected in tissue homogenates of selected brain areas. Finally, a decrease in corticotropin-releasing factor (CRF) mRNA levels was induced by OEA in the central amygdala, while an increase in oxytocin mRNA levels was induced in the PVN. The restoration of a normal oxytocin receptor density in the striatum paralleled the oxytocinergic stimulation produced by OEA. In conclusion, we provide evidence suggesting that OEA might represent a novel potential pharmacological target for the treatment of binge-like eating behavior.

2017 ◽  
Author(s):  
Patricia Westmoreland ◽  
Phillip S Mehler

Feeding and eating disorders are defined by persistent disturbance of eating (or behaviors related to eating) with subsequent changes in consumption or absorption of nutrition that are detrimental to physical health and social functioning. The following eating disorders are described in the DSM-5: anorexia nervosa, bulimia nervosa, binge eating disorder, pica, rumination disorder, avoidant/restrictive food intake disorder (ARFID), other specified feeding or eating disorder (OSFED), and unspecified feeding or eating disorder (USFED). ARFID, OSFED, USFED, rumination disorder, and binge eating disorder are new additions to the manual and are first described in the DSM-5. The DSM-5 also provides severity specifiers—mild, moderate, severe, and extreme—for the diagnoses of bulimia nervosa and anorexia nervosa. This review describes the eating disorders enumerated in the DSM-5 and provides information regarding their genesis and course. This review contains 8 tables and 79 references Key words: avoidant/restrictive eating disorder, binge eating disorder, DSM-5, eating disorder, other specified feeding or eating disorder, pharmacotherapy, pica rumination, psychotherapy, unspecified feeding or eating disorder


CNS Spectrums ◽  
2015 ◽  
Vol 20 (6) ◽  
pp. 537-545 ◽  
Author(s):  
Chiara Giuliano ◽  
Pietro Cottone

Binge eating disorder is characterized by excessive, uncontrollable consumption of palatable food within brief periods of time. Excessive intake of palatable food is thought to be driven by hedonic, rather than energy homeostatic, mechanisms. However, reward processing does not only comprise consummatory actions; a key component is represented by the anticipatory phase directed at procuring the reward. This phase is highly influenced by environmental food-associated stimuli, which can robustly enhance the desire to eat even in the absence of physiological needs. The opioid system (endogenous peptides and their receptors) has been strongly linked to the rewarding aspects of palatable food intake, and perhaps represents the key system involved in hedonic overeating. Here we review evidence suggesting that the opioid system can also be regarded as one of the systems that regulates the anticipatory incentive processes preceding binge eating hedonic episodes.


2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Roseann E. Peterson ◽  
Shawn J. Latendresse ◽  
Lindsay T. Bartholome ◽  
Cortney S. Warren ◽  
Nancy C. Raymond

Despite considerable comorbidity between mood disorders, binge eating disorder (BED), and obesity, the underlying mechanisms remain unresolved. Therefore, the purpose of this study was to examine models by which internalizing behaviors of depression and anxiety influence food intake in overweight/obese women. Thirty-two women (15 BED, 17 controls) participated in a laboratory eating-episode and completed questionnaires assessing symptoms of anxiety and depression. Path analysis was used to test mediation and moderation models to determine the mechanisms by which internalizing symptoms influenced kilocalorie (kcal) intake. The BED group endorsed significantly more symptoms of depression (10.1 versus 4.8,P=0.005) and anxiety (8.5 versus 2.7,P=0.003). Linear regression indicated that BED diagnosis and internalizing symptoms accounted for 30% of the variance in kcal intake. Results from path analysis suggested that BED mediates the influence of internalizing symptoms on total kcal intake (empiricalP<0.001). The associations between internalizing symptoms and food intake are best described as operating indirectly through a BED diagnosis. This suggests that symptoms of depression and anxiety influence whether one engages in binge eating, which influences kcal intake. Greater understanding of the mechanisms underlying the associations between mood, binge eating, and food intake will facilitate the development of more effective prevention and treatment strategies for both BED and obesity.


CNS Spectrums ◽  
2015 ◽  
Vol 20 (6) ◽  
pp. 557-565 ◽  
Author(s):  
Iris M. Balodis ◽  
Carlos M. Grilo ◽  
Marc N. Potenza

Biobehavioral features associated with binge-eating disorder (BED) have been investigated; however, few systematic reviews to date have described neuroimaging findings from studies of BED. Emerging functional and structural studies support BED as having unique and overlapping neural features as compared with other disorders. Neuroimaging studies provide evidence linking heightened responses to palatable food cues with prefrontal areas, particularly the orbitofrontal cortex (OFC), with specific relationships to hunger and reward-sensitivity measures. While few studies to date have investigated non-food-cue responses; these suggest a generalized hypofunctioning in frontostriatal areas during reward and inhibitory control processes. Early studies applying neuroimaging to treatment efforts suggest that targeting neural function underlying motivational processes may prove important in the treatment of BED.


2021 ◽  
Vol 12 ◽  
Author(s):  
Janina Reents ◽  
Anya Pedersen

Overeating behavior is supposedly a major contributing factor to weight gain and obesity. Binge eating disorder (BED) with reoccurring episodes of excessive overeating is strongly associated with obesity. Learning models of overeating behavior and BED assume that mere confrontation with food leads to a conditioned response that is experienced as food craving. Accordingly, individuals with obesity and BED were shown to have high trait food cravings. To date, little is known about differences in state food cravings and cue reactivity at the sight of palatable food in individuals with obesity and BED compared to individuals with obesity without BED. Therefore, the aim of our study was to examine differences in cue-induced, state and trait food cravings in people with obesity with and without BED. We found that all aspects of food cravings were more prevalent in individuals with obesity and BED than in individuals without BED. By implementing a food cue reactivity paradigm, our results show that individuals with obesity with BED have more cue-induced cravings than individuals with obesity without BED. Moreover, these cue-induced cravings in individuals with obesity and BED were highest for high-fat and high-sugar foods as opposed to low-calorie foods. Thus, our results emphasize the role of increased cue reactivity and craving at the sight of palatable foods in individuals with obesity and BED. Hence, our findings support etiological models of conditioned binge eating and are in line with interventions targeting cue reactivity in BED.


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