Metabolic-associated liver disease (MAFLD) affects up to 70% of overweight and more than 90% of morbidly obese people, and its pathogenesis is rather complex and multifactorial. The criteria for MAFLD include the presence of hepatic steatosis in addition to one of the following three criteria: overweight or obesity, presence of type 2 diabetes mellitus (T2DM), or evidence of metabolic dysregulation. If the specific criteria are present, the diagnosis of MAFLD can be made regardless of alcohol consumption and previous liver disease. The pathophysiological mechanisms of MAFLD, including inflammation, lipotoxicity, mitochondrial disfunction, and oxidative stress, as well as the impact of intestinal gut microbiota, are constantly being elucidated. Treatment strategies that are continually emerging are based on different key points in MAFLD pathogenesis. Yet, the ideal therapeutic option has still not been found and future research is of great importance, as MAFLD represents a multisystemic disease with numerous complications.

Non-alcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease which is characterized by extremely complex pathogenetic mechanisms and multifactorial etiology. Some of the many pathophysiological mechanisms involved in the development of NAFLD include oxidative stress, impaired mitochondrial metabolism, inflammation, gut microbiota, and interaction between the brain-liver-axis and the regulation of hepatic lipid metabolism. The new therapeutic approaches in the treatment of NAFLD are targeting some of these milestones along the pathophysiological pathway and include drugs like agonists of peroxisome proliferator-activated receptors (PPARs), glucagon-like peptide-1 (GLP-1) agonists, sodium/glucose transport protein 2 (SGLT2) inhibitors, farnesoid X receptor (FXR) agonists, probiotics, and symbiotics. Further efforts in biomedical sciences should focus on the investigation of the relationship between the microbiome, liver metabolism, and response to inflammation, systemic consequences of metabolic syndrome.

Early life adversities leave long-lasting structural and functional consequences on the brain, which may persist later in life. Dopamine is a neurotransmitter that is extremely important in mood and motor control. The aim of this study was to investigate the effect of maternal deprivation during the ninth postnatal day on the volume of dopaminergic nuclei and the number of dopaminergic neurons in adolescence and adulthood. Maternally deprived and control Wistar rats were sacrificed on postnatal day 35 or 60, and the dopaminergic neurons were stained in coronal histological sections of ventral midbrain with the tyrosine hydroxylase antibody. The volume of dopaminergic nuclei and the number of dopaminergic neurons in the substantia nigra (SN) and ventral tegmental area (VTA) were analyzed in three representative coordinates. Maternal deprivation caused weight loss on postnatal day 21 (weaning) and corticosterone blood level elevation on postnatal days 35 and 60 in stressed compared to control rats. In maternally deprived animals, the volumes of SN and VTA were increased compared to the controls. This increase was accompanied by an elevation in the number of dopaminergic neurons in both nuclei. Altogether, based on somatic and corticosterone level measurements, maternal deprivation represents a substantial adversity, and the phenotype it causes in adulthood includes increased volume of the dopaminergic nuclei and number of dopaminergic neurons.

The insular cortex has emerged as a key region implicated in a wide array of cognitive, emotional, and sensory processes. The anterior part of the insula (AIC) is central to emotional awareness, decision-making, and interoception, while the posterior insula (PIC) is more associated with somatosensory processing. The insula acts as a functional hub within the salience network and integrates homeostatic, affective, and cognitive information; thus, its role in different mental disorders seems to be prominent. Altered structure and connectivity of the insular cortex are evident in several psychiatric conditions. In schizophrenia, reductions in insular volume—especially on the left—correlate with hallucinations, emotional dysregulation, and cognitive deficits. Bipolar and major depressive disorders exhibit AIC volume loss and aberrant connectivity patterns linked to impaired affect regulation and interoceptive awareness. Anxiety disorders show functional hyperactivity of the insula, especially in response to fear-inducing stimuli, though findings on structural changes are mixed. Overall, growing evidence underscores the insular cortex’s central role in psychiatric pathophysiology and highlights its potential as a target for future diagnostic and therapeutic strategies.

Obstructive sleep apnea (OSA) is characterized by repetitive complete or partial collapse of the upper airway and reduction of airflow during sleep. It is associated with significantly increased daytime muscle sympathetic nerve activity thought to result from the repetitive intermittent periods of hypoxemia during sleep and brain alterations that are likely to result. Different brain regions are affected by subsequent hypoxia/anoxia. Neurodegenerative processes result in measurable atrophy of cortical gray matter in the temporal lobes and posterior cingulate cortex, as well as in subcortical structures such as the hippocampus, amygdala, and thalamus. This study involved a group of firstly diagnosed, therapy-naive, nonalcoholic fatty liver disease (NAFLD) patients, out of which 144 (96 males and 48 females), aged 34–57 (mean 47.88 ± 6.07), satisfied the recruiting criteria for the study and control groups. All the patients underwent MRI scanning, polysomnography testing, and cognitive evaluation. Cognitively, worse results were obtained in the group with OSA (p < 0.05) and NAFLD (p = 0.047). A significant decrease in volumes of cortical and subcortical structures was revealed (p < 0.001). In conclusion, brain deterioration followed by cognitive impairment is, most likely, the result of intermittent hypoxia and anoxia episodes that initiate the domino process of deteriorating biochemical reactions in the brain.

Background / Aim. The sciatic nerve (SN) is a mixed nerve formed in pelvis by joining of L4 - S3 anterior spinal nerve roots. SN can be under the pressure in different regions throughout its course. However, the most frequent site of impingement is under the piriformis muscle which causes the occurrence of piriformis syndrome. High division of SN has its relevance considering the fact that it leads to the compression of nerve resulting in piriformis syndrome. The aim of this study was to determine the connection be-tween anatomical parameters of pelvis and high division of SN, which is considered to be one of the most common causes of piriformis syndrome in both genders. Methods. This study was conducted on 28 formalin fixed cadavers of both genders at the Institute of Anatomy, Faculty of Medicine, University of Belgrade (Belgrade, Serbia) and the Department of Anatomy, School of Medicine, University of St Andrews (St Andrews, United Kingdom). For the measuring of required dimensions, we used a ruler and a caliper. Results. A statistically significant difference in the values of bispinal and bituberal lines was observed. A high division of SN was found on 58.33% of the male cadavers and 80% of the female cadavers. A statistically significant difference in the mean value of the bituberal line between the male and female sex was also recognised. Conclusion. The connection between the anatomical parameters of the pelvis and the level of division of the SN is confirmed. Although on the basis of the results it could be assumed that people with smaller pelvic dimensions would have greater likelihood of developing a piriformis syndrome, the other factors, such as biomechanics related to a wider ?Q angle? in women that could result in a higher incidence of piriformis syndrome, should also be considered.