👤 Krisztina Horváth

Problematic social media use (PSMU) has emerged as a societal and behavioral concern, especially among young adults. However, individual differences in symptom manifestation remain understudied. The present study adopted a person-centered approach to identify distinct profiles of PSMU and to examine the predictive roles of fear of missing out (FoMO), problematic smartphone use (PSU), age, and sex among a sample of 625 Italian university students aged 18 to 40 years ( Show less

Fasting triggers complex physiological and neuroimmune adaptations, yet its impact on hypothalamic microglia and the underlying regulatory role of glucocorticoids remains incompletely understood. The present study focused on fasting-induced systemic changes and cellular adaptations seen in the hypothalamus where components of metabolic- hormonal- and immune regulations are integrated. Adult male microglia reporter (CX3CR1 Overnight fasting resulted in a decrease in energy expenditure and respiratory exchange ratio (RER) indicating conservation of energy and a metabolic shift towards utilization of fatty acids as alternative energy source. Fasting increased hypothalamic expression of orexigenic neuropeptides and mRNA levels of Pdk4, Glut1, and Mct2 genes, in line with metabolic compensation. Upregulation of hypothalamic Crh and increased plasma concentration of corticosterone indicated sustained activation of the HPA axis. Importantly, fasting promoted an anti-inflammatory milieu in the hypothalamus characterized by elevated Il-4, Il-10 and IkBα genes without significant activation of pro-inflammatory cytokines (e.g., Il-1β, Il-6, Tnfα). Morphological analysis revealed region-specific changes in microglia number and branching complexity, particularly in hypothalamic regions directly exposed to blood-borne signals. Functional profiling showed increased microglial expression of IkBα and decreased pIkBα, indicating suppressed NFkB signaling. Adrenalectomy (1 week) and acute pharmacological inhibition of corticosterone synthesis (methyrapone) revealed that fasting-induced anti-inflammatory and metabolic gene expression, as well as microglial plasticity were largely glucocorticoid dependent. Hypothalamic expression of fasting-related neuropeptides (Npy, Agrp) and genes, related to the metabolic shift (Pdk4, Glut-1, Mct2, Angptl4) as well as some immune-related genes (Il10, Iba1) was dependent on presence of the adrenal gland or fasting-induced elevation of corticosterone. These findings highlight short term fasting as a potent modulator of hypothalamic immune-metabolic crosstalk and reveal critical role of adrenal glucocorticoids in orchestrating microglial responses to energetic challenges. The results have potential implications for therapeutic interventions targeting metabolic and inflammatory disorders. Show less

Obesity is a global health challenge that can lead to various complications, such as metabolic syndrome, diabetes mellitus, and cardiovascular diseases. Heat shock proteins are evolutionarily conserved chaperones that help maintain cellular protein homeostasis. Their expression is dysregulated in various chronic diseases, including diabetes mellitus and hyperlipidemia, and they also regulate inflammatory processes. Therefore, the present study aimed to investigate the effects of a small heat shock protein, HSPB1, on the comorbidities and complications of obesity in a transgenic mouse model. Male and female human apolipoprotein B-100 (APOB) transgenic mice fed with a high-fat diet (HFD) from months 3-10 of age were used as a model of metabolic syndrome (MetS). To study whether HSPB1 influences the development of MetS, APOB animals were crossed with HSPB1-overexpressing mice. Age and sex-matched wild-type and human HSPB1-overexpressing mice were used as controls. Changes in cardiac morphology and function were assessed by transthoracic echocardiography at month 9. At month 10, serum triglyceride and cholesterol concentrations were determined by enzymatic colorimetric assays. Pathological changes in the liver were studied on hematoxylin-eosin-stained sections. Expression levels of genes involved in inflammation and metabolism were measured by quantitative real-time polymerase chain reaction in the liver, left ventricle, and visceral white adipose tissue (vWAT). The body weight and serum LDL-cholesterol levels were significantly higher in the APOB animals than in the wild-type mice in both sexes. Notably, HSPB1 overexpression further increased weight gain in female APOB animals. Conversely, in APOB males, HSPB1 overexpression decreased LDL-cholesterol levels without significantly affecting body weight. Furthermore, in APOB females, HSPB1 overexpression elevated Fgf-21 expression in the vWAT, restored Lpl levels, and reduced the expression of several cytokines in the liver. APOB males developed left ventricular hypertrophy (LVH) with diastolic dysfunction. HSPB1 overexpression induced LVH without cardiac dysfunction in the wild-type animals. Both sexes of APOB animals developed MetS. APOB males presented LVH with preserved ejection fraction (EF); however, APOB females showed enlarged left ventricular end-systolic volume (LVESV). In APOB animals, HSPB1 overexpression exerted a sex-dependent influence on obesity-related alterations, including weight gain, hypercholesterolemia, and hepatic and vWAT gene expression. Show less