Apelin-13 and Asprosin in Adolescents with Anorexia Nervosa and Their Association with Psychometric and Metabolic Variables.

Anorexia nervosa (AN) is a widespread, metabo-psychiatric disorder with high relapse rates, comorbidity, and mortality. Many regulatory proteins and neurohormones studied to date play essential roles in the etiopathogenesis of eating disorders and the maintenance of psychopathological symptoms. Nevertheless, the regulatory and pathophysiological mechanisms of AN are still poorly understood. In the presented study, the plasma levels of apelin-13 (APE-13) and asprosin (ASP), as well as carbohydrate metabolism parameters and psychometric parameters, were evaluated in low-weight adolescent female patients with AN (AN1), after partial weight normalization (AN2) and in an age-matched healthy control group (CG) were evaluated. APE-13 levels were higher in the AN1 group than in the post-realimentation and the CG group. APE-13 levels were independent of insulin and glucose levels. Plasma ASP levels increased with increasing body weight in patients with AN, correlating with the severity of eating disorder symptoms in emaciation. The presented data suggest that APE-13 and ASP may be AN's biomarkers-regulation of eating behavior by APE-13 and ASP, the close relationship between them and emotional behavior, and changes in neurohormone levels in patients with eating and affective disorders seem to support these hypotheses. Moreover, their plasma levels seem to be related to the severity of psychopathological symptoms of eating disorders.

The Effect of Physical Activity on Neurotrophin Concentrations and Cognitive Control in Patients With a Depressive Episode.

Background: Cognitive deficits occur in most patients with affective disorders. The role of neurotrophic factors (e.g., BDNF) as modulators of brain plasticity affecting neurocognitive abilities has been emphasized. Neurotrophin concentrations may change under the influence of various interventions, including physical activity. Selected studies have shown that cognitive function may also be affected by exercise. Aim: The aim of the study was to determine whether physical activity changes the concentration of neurotrophins and their receptors in patients with an episode of depression. It was also examined how one session of aerobic exercise affects cognitive control. Methods: The study included 41 participants. The subjects were asked to exercise on a cycloergometer for 40 min with individually selected exercise loads (70% VO2max). Before and shortly after the exercise blood samples were acquired to perform blood assays (proBDNF, BDNF, TrkB, NGFR). The participants also performed a Stroop test twice-before the exercise and 10 min after its cessation. Results: The single bout of physical exercise did not cause any significant changes in the concentration of neurotrophic factors. The SCWT results: both the mean reading time (29.3 s vs. 47.8 s) and the color naming time (36.7 s vs. 50.7 s) increased. The patients made more mistakes after physical exercise, both in part A (0.2 vs. 1.5) and B (0.6 vs. 1.5). The so-called interference effect decreased-the difference between naming and reading times was smaller after exercise (6.2 s vs. 2.4 s). No significant correlations were found between the concentrations of the studied neurotrophic factors and the Stroop test results. Conclusions: The results did not confirm changes in neurotrophin concentration under the influence of a single session of physical activity. The shortening of the interference time after exercise may be caused by practice effects. A significant limitation of the study is the use of the Stroop test twice in short intervals.

Augmentation of Pharmacotherapy by Sleep Deprivation with Sleep Phase Advance in Treatment-Resistant Depression.

INTRODUCTION: The aim was to assess the efficacy of total sleep deprivation (TSD) with sleep phase advance (SPA) in treatment-resistant depression (TRD) and associated biochemical factors. METHODS: We studied nine males and 12 females, aged 49±14 years, with treatment-resistant unipolar or bipolar depression, receiving antidepressant and mood-stabilizing drugs. The four-day schedule included single TSD and three consecutive nights with SPA. Biochemical markers were measured on the day before and on 1st, 7th and 14th day after the TSD. RESULTS: Ten subjects met criteria for response, defined as a reduction of ≥50% in the Hamilton Depression Rating Scale, on the 14th day. Concentrations of cortisol at baseline were lower in responders, and they decreased during therapy in both groups. In responders, there was an increase of interleukin-10 (IL-10) and IL-1ß on the 14th day. DISCUSSION: Our preliminary study demonstrated the efficacy of pharmacotherapy augmentation by TSD and SPA in half of the patients with TRD. The main biochemical factors related to clinical response included status of cortisol and increase in IL-10 and IL-1ß levels.