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Background: Obese patients (Ob) with a binge eating disorders (BED) behavior pattern have a higher prevalence of postprandial distress syndrome (PDS) compared to Ob without a BED behavior pattern, while an increase of PDS has been
Obesity-induced changes in the metabolic and endocrine milieu elicit deficits in neuroplasticity, including increased risk for development of neuropsychiatric disorders such as depressive illness. We previously demonstrated that downregulation of hypothalamic insulin receptors (hypo-IRAS) elicits a
Obesity, besides being a problem of metabolic dysfunction, constitutes a risk factor for psychological disorders. Experimental models of diet-induced obesity have revealed that obese animals are prone to anxious and depressive-like behaviors. The present study aimed to evaluate whether
The aim of this study was to evaluate differences in body mass index and eating behavior in obese and overweight persons with and without anhedonia during a weight loss intervention study. Psychiatric diagnostics were based on the Structured Clinical Interview for DSM-IV disorders. Eating behavior
Anhedonia and abnormalities in reward behavior are core features of major depressive disorder (MDD). Convergent evidence indicates that overweight/obesity (OW), a highly prevalent condition in MDD, is independently associated with reward disturbances. We therefore aimed to investigate The purpose of the study was to examine the rate of alexithymia as measured by the Toronto Alexithymia Scale in a sample of severely obese subjects, as well as the relationships between this dimension and five other dimensions found in obesity: depression, anhedonia, external locus of control,
OBJECTIVE
Depressive symptoms in adolescents have been associated with reduced physical activity. However, existing studies have relied on questionnaire measures of physical activity, which may not necessarily reflect actual energy expenditures. We sought to evaluate the relationship between
Nesfatin-1 is a well-established anorexigenic peptide. Recent studies indicated an association between nesfatin-1 and anxiety/depression-like behavior. However, it is unclear whether this effect is retained in obesity. The aim was to investigate the effect of nesfatin-130-59-the active
OBJECTIVE
To examine whether a diagnosis for major depression, chronic depression or specific symptoms of depression is associated with the risk of quitting a weight loss program.
METHODS
The study involved 82 overweight adults participating in the Lifestyle Intervention Treatment Evaluation (LITE)
Excessive consumption and obesity do not always have to be strictly pathological. The adjustment of food intake as well as the pleasure of eating are the results of the circulation of neurotransmitters, hormones and glucocorticoids which have an ability to regulate the activity of many receptors
Diet-induced obesity (DIO) causes ghrelin resistance in hypothalamic Agouti-related peptide (AgRP) neurons. However, ghrelin promotes feeding through actions at both the hypothalamus and mesolimbic dopamine reward pathways. Therefore, we hypothesized that DIO would also establish ghrelin resistance
Depression, together with insulin resistance, is increasingly prevalent among youth. These conditions have traditionally been compartmentalized, but recent evidence suggests that a shared brain motivational network underlies their co-occurrence. We posit that, in the context of depressive symptoms,
Objectives: Imbalanced nutrition and obesity are risk factors for depression, a relationship that in rodents can be modeled by depression-like behavior in response to high-fat diet (HFD). In this work, we examined the role of the intestinal microbiota and the adipocytokine leptin as potential
Alterations in endocrine functions and low-grade systemic inflammation represent fundamental characteristics of obesity. These biological systems have been repeatedly linked to fatigue symptoms. The aim of the study was to assess the relationship between fatigue dimensions and metabolic/inflammatory
There is a well-established literature linking obesity to altered dopamine signaling and brain response to food-related stimuli. Neuroimaging studies frequently report enhanced responses in dopaminergic regions during food anticipation and decreased responses during reward receipt. This has been