17,252 research outputs found
Effect of oleoylethanolamide in an animal model of binge eating and in a model of reinstatement of high-fat food seeking.
No full textOleoylethanolamide (OEA), is an endogenous lipid, which, despite its structural and similar biosynthetic pathways to anandamide, shows opposite effects on feeding and lipid metabolism regulation. In the recent years, OEA has clearly emerged as a potential novel pharmacological target for the development of therapies aimed at controlling aberrant eating patterns, such as those causing obesity and/or eating disorders.
The main purpose of this study was to evaluate the effect of OEA in an animal model of binge eating and in a model of self administration of high-fat food and reinstatement of high-fat food seeking, after extinction.
Binge eating episodes are characterized by uncontrollable, distressing eating of a large amount of highly palatable food.
These episodes represent a central feature of bingeing-related eating disorders, such as binge eating disorder, bulimia nervosa, and binge/purge subtype anorexia nervosa.
In our animal model of binge eating we used four groups of female rats that were first exposed or not exposed to repeated
intermittent cycles of regular chow food restriction during which they were also given intermittent access to highly
palatable food. On the test day, we either exposed or did not expose the rats to the sight of the palatable food for 15 min
(frustration stress) before assessing food consumption for 2 h.
To investigate the effect of stress-induced relapse to unhealthy eating habits during dieting, we adapted a rat reinstatement
model, commonly used to study relapse to abused drugs.
OEA showed its anorectic action in the preclinical models, these effects could be due to the induction of satiety and activation of the nuclear receptor PPAR-alpha, being considered an endogenous agonist for this activity.
Moreover, since the administration of OEA induces an increase in expression and neurosecretion of oxytocin in the hypothalamus, the increase of this hormone in our animal models may mediate the downregulation of CRF system, involved in the episodes of binge eating and in reinstatement of palatable food seeking.
In conclusion, OEA could be a promising candidate for the treatment of these maladaptive eating habits
The Story of "Me" Contemporary American Autofiction
No full textCover -- Title Page -- Copyright Page -- Contents -- Acknowledgments -- Introduction -- 1. Masculinity, Whiteness, and Postmodern Self-Consciousness -- 2. Rage against the Dying of the Author -- 3. The New Journalism as the New Fiction -- 4. Trauma Autofiction, Dissociation, and the Authenticity of "Real" Experience -- 5. Memoir vs. Autofiction as the Story of Me vs. the Story of "Me" -- Coda -- Appendix -- Notes -- References -- IndexDescription based on publisher supplied metadata and other sources.Electronic reproduction. Ann Arbor, Michigan : ProQuest Ebook Central, YYYY. Available via World Wide Web. Access may be limited to ProQuest Ebook Central affiliated libraries
Central effects of the satiety signal oleoylethanolamide in an animal model of frustration stress-induced binge eating disorder
No full textBinge-eating disorder (BED), characterized by compulsive and uncontrollable overeating of highly palatable food (HPF), has been associated to altered dopamine (DA) and serotonin (5-HT) brain signalling. The satiety signal oleoylethanolamide (OEA) has emerged as a potential novel pharmacological tool for controlling aberrant eating patterns, by restoring a normal brain dopaminergic response, when it is deregulated by an excessive dietary fat intake. Based on these premises in this study we investigated in a rat model of BED the effects of OEA: 1) on Fos expression and tissue monoamine (DA, 5-HT, Noradrenaline) concentrations in brain areas controlling feeding and reward; 2) on the modulation of DA release within the shell of the nucleus accumbens (AcbSh). In our model, female rats with a history of intermittent food restriction and HPF consumption showed binge-like food intake after the exposure to a “frustration stress” consisting of the sight of unreachable HPF (BED rats). Control rats were exposed to the same experimental manipulations except for food restriction and did not show any binge eating behaviour. OEA was administered (10 mg/kg i.p.) to two different sets of both BED and control rats. A first set was sacrificed 2 hours after OEA administration; their brains were partly sliced into 20 μm coronal sections (immunostained for Fos), and partly microdissected for monoamine determination by HPLC.The second set of rats was subjected to in vivo microdialysis of the AcbSh, collecting dialysates every 15 min, and was first intraperitoneally treated with OEA (10 mg/kg) and then challenged with a subcutaneous dose of amphetamine (0.5 mg/kg). DA dialysate levels were analysed by HPLC. OEA administration was able to restore a “normal” brain activity, by reducing the stress-induced Fos increase in brain areas regulating feeding and the dopaminergic signalling. Moreover, we found that OEA treatment decreased DA efflux in the AcbSh, following either stress exposure or amphetamine challenge. At tissue level, we found that OEA also reduced DA concentration within the Acb of BED rats. As far as the serotonergic system, we found that OEA is able to enhance 5-HT transmission in most of the brain areas analysed, selectively in bingeing rats. Overall, these results further enrich our current knowledge on the central effects of OEA and support, for the first time, the hypothesis that OEA might represent a novel potential pharmacological target for the treatment of BED
Epigenetic regulation of adenosine A2A and dopamine D2 receptor gene transcription on compulsive food consumption
No full textDifferent regulation of prodynorphin and pronociceptin genes expression in resistance to diet-induced obesity
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Satiety factor oleoylethanolamide prevents binge-like palatable food consumption induced by stress in female rats with a history of food restriction
No full textEpigenetic regulation of nociceptin/orphanin FQ and corticotropin-releasing factor system genes in frustration stress-induced binge-like palatable food consumption
No full textEvidence suggests that binge eating may be caused by a unique interaction between dieting and stress. We developed a binge-eating model in which female rats with a history of intermittent food restriction show binge-like palatable food consumption after a 15-minute exposure to the sight of the palatable food (frustration stress). The aim of the present study was to investigate the regulation of the stress neurohormone corticotropin-releasing factor (CRF) system and of the nociceptin/orphanin FQ (N/OFQ) system genes in selective rat brain regions, using our animal model. Food restriction by itself seems to be responsible in the hypothalamus for the downregulation on messenger RNA levels of CRF-1 receptor, N/OFQ and its receptor (NOP). For the latter, this alteration might be due to selective histone modification changes. Instead, CRF gene appears to be upregulated in the hypothalamus as well as in the ventral tegmental area only when rats are food restricted and exposed to frustration stress, and, of relevance, these changes appear to be due to a reduction in DNA methylation at gene promoters. Moreover, also CRF-1 receptor gene resulted to be differentially regulated in these two brain regions. Epigenetic changes may be viewed as adaptive mechanisms to environmental perturbations concurring to facilitate food consumption in adverse conditions, that is, in this study, under food restriction and stressful conditions. Our data on N/OFQ and CRF signaling provide insight on the use of this binge-eating model for the study of epigenetic modifications in controlled genetic and environmental backgrounds
Epigenetic regulation of hypothalamic neuropeptides gene expression in diet induced obesity resistant rats
No full textA variety of factors plays a role in obesity (i.e. behavior, environment, and genetics) and epigenetic regulation of gene expression has emerged as a potential contributor in the susceptibility and development of obesity. To investigate the individual sensitivity to weight gain/resistance, we here studied genes transcription regulation of hypothalamic neuropeptides involved in the control of energy balance in rats developing (diet-induced obese, DIO) or not obesity (diet resistant, DR), when fed with a high fat diet (HFD). Rats have been followed up to 21 weeks of HFD exposure. After 5 weeks HFD exposure, the obese phenotype has been developed and we observed a selective down-regulation of the orexygenic neuropeptide Y (NPY) and peroxisome proliferatoractivated receptor gamma (PPAR-γ) genes and no changes for the agouti-related protein (AgRP), as well as for all the anorexigenic genes under study. After long-term HFD exposure (21 weeks), NPY and PPARγ, as well as most of the genes under study, resulted not to be different between DIO and DR whereas a lower expression of the anorexigenic pro-opio-melanocortin (POMC) gene in DIO rats when compared to DR. We also observed that changes in NPY and POMC mRNA were inversely correlated with gene promoters DNA methylation. Our findings suggest that selective alterations in hypothalamic peptide genes regulation could contribute to the development of overweight in rats and that environmental factor, as in this animal model, might be partially responsible of these changes via epigenetic mechanism
Effects of Oleoylethanolamide on mesolimbic dopaminergic transmission in an animal model of binge eating.
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