Stress, together with dieting and negative affects, is a common trigger of eating disorders. Binge-eating (BE) disorder is characterized by the consumption of an unusual large amount of food associated with the sense of loss of control over eating during the episode. The physiological control of BE is extremely complex, involving a balance of both central and peripheral neurotransmitters and neuropeptides that interact to stimulate or inhibit food intake. The endocannabinoid (eCB) system has long been known as a modulator of physiological functions and plays an important role in brain circuits related to feeding behaviours. We analyzed the transcriptional regulation of eCB system genes in selected brain regions (Amygdala complex, Caudate Putamen (CP), Nucleus Accumbens, Hypothalamus (HY) and Ventral Tegmental Area) of an animal model of BE which combines cycles of food restriction/refeeding and acute stress to evoke BE for sweet high palatable food. Analysis in the HY of stressed and exposed to restriction rats revealed a significant selective decrease of Fatty Acid Amide Hydrolase mRNA when compared to the other groups. Moreover in the CP of stressed rats exposed or not to restriction it was observed a significant decrease of gene expression of both Cannabinoid receptor type-2 and type-3 respect to no stressed rat as well as of Vanilloid Receptor 1 in the stressed and restricted group respect to non-stressed and non-restricted rats. No changes were observed in the other brain regions analyzed. We here provide evidence of how the exposure to stress and cycles of intermittent food restriction produced selective changes of eCB elements in the HY and in the CP. Further studies are needed to clarify the involvement of eCB system in regulation and development of BE disorder focusing on the role of environmental factors in the development of BE episodes and thus on the epigenetic mechanisms triggering the observed changes in genes expression.
Characterization of endocannabinoid system in an animal model of binge eating
Micioni Di Bonaventura MV;Cifani C;
2017-01-01
Abstract
Stress, together with dieting and negative affects, is a common trigger of eating disorders. Binge-eating (BE) disorder is characterized by the consumption of an unusual large amount of food associated with the sense of loss of control over eating during the episode. The physiological control of BE is extremely complex, involving a balance of both central and peripheral neurotransmitters and neuropeptides that interact to stimulate or inhibit food intake. The endocannabinoid (eCB) system has long been known as a modulator of physiological functions and plays an important role in brain circuits related to feeding behaviours. We analyzed the transcriptional regulation of eCB system genes in selected brain regions (Amygdala complex, Caudate Putamen (CP), Nucleus Accumbens, Hypothalamus (HY) and Ventral Tegmental Area) of an animal model of BE which combines cycles of food restriction/refeeding and acute stress to evoke BE for sweet high palatable food. Analysis in the HY of stressed and exposed to restriction rats revealed a significant selective decrease of Fatty Acid Amide Hydrolase mRNA when compared to the other groups. Moreover in the CP of stressed rats exposed or not to restriction it was observed a significant decrease of gene expression of both Cannabinoid receptor type-2 and type-3 respect to no stressed rat as well as of Vanilloid Receptor 1 in the stressed and restricted group respect to non-stressed and non-restricted rats. No changes were observed in the other brain regions analyzed. We here provide evidence of how the exposure to stress and cycles of intermittent food restriction produced selective changes of eCB elements in the HY and in the CP. Further studies are needed to clarify the involvement of eCB system in regulation and development of BE disorder focusing on the role of environmental factors in the development of BE episodes and thus on the epigenetic mechanisms triggering the observed changes in genes expression.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
