Obesity-related disruption in lipid metabolism contributes to cardiovascular dysfunction. Despite numerous studies on lipid metabolism in the left ventricle, there is no data describing the influence of n-acetylcysteine (NAC) and α-lipoic acid (ALA), as glutathione precursors, on sphingolipid metabolism, and insulin resistance (IR) occurrence. The aim of our experiment was to evaluate the influence of chronic antioxidants administration on myocardial sphingolipid state and intracellular insulin signaling as a potential therapeutic strategy for obesity-related cardiovascular IR. The experiment was conducted on male Wistar rats fed a standard rodent chow or a high-fat diet with intragastric administration of NAC or ALA for eight weeks. Cardiac and plasma sphingolipid species were assessed by high-performance liquid chromatography (HPLC). The proteins expressed from sphingolipid and insulin signaling pathways were determined by Western blot. Antioxidant supplementation markedly reduced ceramide accumulation by lowering the expression of selected proteins from the sphingolipid pathway and simultaneously increased the myocardial sphingosine-1-phosphate level. Moreover, NAC and ALA augmented the expression of GLUT4 and the phosphorylation state of Akt (Ser473) and GSK3β (Ser9), which improved the intracellular insulin transduction pathway. Based on our results, we may postulate that NAC and ALA have a beneficial influence on the cardiac ceramidose under IR conditions.

Patients suffering from childhood acute lymphoblastic leukemia (ALL) are at risk of late adverse treatment-related effects. The examination of targeted biomarkers could be used to improve the diagnosis and prediction of life-threatening ALL sequelae. The purpose of this cross-sectional study was to search for treatment-related alterations in apolipoprotein (Apo) levels as potential markers of the occurrence of obesity in subjects treated for ALL, and to assess the relationships between weight, gender, anticancer treatment, and Apo concentrations. Fifty-eight ALL survivors were included in the study. The mean time of follow-up after treatment cessation was 5.41 ± 4.29 years. Serum levels of apolipoproteins were measured using a multiplex assay kit. Among ALL survivors, we observed a significant correlation of Apo-C1, Apo-C3, Apo-H, and Apo-J levels, depending on body mass index (BMI). Marked differences were observed in the area under the curve of Apo-A1, Apo-A2, Apo-C1, Apo-D. In our study, patients with a history of childhood ALL developed alterations in their Apo profile. Furthermore, this is the first study revealing that some apolipoproteins may act as valuable biomarkers useful in the prognosis of metabolic imbalance. We believe that this paper, at least partially, will highlight the importance of long-term prognosis of metabolic complications associated with the anticancer chemotherapy used to treat hematological malignancies in children.

Background: Psoriasis is a chronic, multi-system inflammatory disease frequently associated with metabolic syndrome and lipid disturbances. Apolipoproteins, as essential regulators of lipid metabolism, may play a critical role in these metabolic abnormalities, potentially influencing disease severity and systemic inflammation. The aim of this study was to compare serum concentrations of chosen apolipoproteins in patients with psoriasis before and after treatment with acitretin or narrowband UVB (NB-UVB). Methods: This study was conducted on 39 patients with psoriasis. The concentration of nine apolipoproteins and C-reactive protein was quantified using the Bio-Plex Immunoassay Kit. Results: The serum concentrations of ApoA2, ApoC1, ApoD, ApoE, and ApoJ were higher in the acitretin group compared to the NB-UVB group before treatment, while the ApoA1/ApoA2 ratio was lower. We also observed a negative association between the Psoriasis Area and Severity Index (PASI) and ApoA1/ApoA2 ratio in the patients before the treatment. Conclusions: The results of this study confirm the presence of metabolic disturbances in psoriatic patients. The treatment with NB-UVB or acitretin did not cause any significant changes in the apolipoproteins profile. Thus, we found no detrimental impact of acitretin on the apolipoproteins profile, despite the observed rise in total cholesterol concentration after the treatment. Further research is needed to explore whether specific therapeutic approaches can modify these disturbances and potentially improve long-term cardiovascular outcomes in this population.

Aerobic exercise training (AET) and numerous dietary interventions, including nitrate and resveratrol supplementation, display overlapping mechanisms affecting mitochondrial bioenergetics and metabolism in diverse tissues. However, it remains unclear if a combination of these interventions results in additive benefits for the prevention of obesity-related co-morbidities. To investigate this, C57Bl/6N mice consumed a high-fat diet and remained sedentary (HFD) or performed AET for 6 weeks in the absence (HFD+AET) or presence of nitrate+resveratrol supplementation (HFD+AET+NR). As expected, AET attenuated body weight gain, reduced adipocyte cross-sectional area and markers of cellular stress/inflammation within white adipose tissue, and increased mitochondrial respiratory capacity and decreased lipid content within skeletal muscle independent of supplementation. While AET alone was sufficient to improve glucose tolerance, the addition of +NR provided modest liver-specific enhancements including increased mitochondrial respiratory capacity, reduced reactive lipid accumulation, and a unique proteomic signature associated with altered amino acid metabolism, corresponding to further reductions in systemic fasting blood glucose levels. These data suggest that while AET remains a primary lifestyle intervention to drive metabolic improvements during high-fat feeding, targeted dietary supplementation may provide tissue-specific enhancements, particularly within the liver, that complement exercise adaptations.