The prolonged consumption of a high-fat diet (HFD) leads to abnormal growth of the visceral adipose tissue (VAT), increased macrophage infiltration, and altered secretion of biologically active molecules. This is considered as a precondition for the development of obesity, inflammation, and obesity-related disorders. Therefore, we studied HFD-induced changes in the tissue levels of the inflammatory markers C-reactive protein, serum amyloid-A, and interleukin-4 in healthy male Wistar rats. The animals were first divided at random into two groups subjected to either a standard or a high-fat diet. The initial effect of the diet was evaluated after fourteen weeks. In order to study the diet duration effect, the standard diet was given to twelve animals from the HFD group, while the remaining continued with the HFD for an additional four weeks. Our results showed that the HFD barely affected body mass index, conicity, relative fat mass, and Lee indices, whereas it provoked adipocyte hypertrophy and gradually increased the levels of both the pro- and anti-inflammatory markers. The switch from the high-fat to the standard diet resulted in the comparatively fast restoration of the baseline levels of the studied molecules. Although, the prolonged consumption of an HFD causes adipocyte hypertrophy in healthy male animals, the inflammatory process in VAT is well-coordinated, time-dependent, and reversible.

Diabetic cardiomyopathy is a major etiological factor in heart failure in diabetic patients, characterized by mitochondrial oxidative metabolism dysfunction, myocardial fibrosis, and marked glycogen elevation. The aim of the present study is to evaluate the effect of endurance training and prebiotic xylooligosaccharide (XOS) on the activity of key oxidative enzymes, myocardial collagen, and glycogen distribution as well as some serum biochemical risk markers in streptozotocin-induced type 1 diabetic rats. Male Wistar rats (n = 36) were divided into four diabetic groups (n = 9): sedentary diabetic rats on a normal diet (SDN), trained diabetic rats on a normal diet (TDN), trained diabetic rats on a normal diet with an XOS supplement (TD-XOS), and sedentary diabetic rats with an XOS supplement (SD-XOS). The results show that aerobic training managed to increase the enzyme activity of respiratory Complex I and II and the lactate dehydrogenase in the cardiomyocytes of the diabetic rats. Furthermore, the combination of exercise and XOS significantly decreased the collagen and glycogen content. No significant effects on blood pressure, heart rate or markers of inflammation were detected. These results demonstrate the beneficial effects of exercise, alone or in combination with XOS, on the cardiac mitochondrial enzymology and histopathology of diabetic rats.

Objectives: Type 1 diabetes mellitus is a metabolic disease characterized by dysbiosis. Modulation of the gut microbiota by oligosaccharides and aerobic training are proposed mechanisms that ameliorate the disease through affecting host-microbiota interactions. Methods: Seventy-two male Wistar rats were randomly divided into 8 groups – 5 with streptozotocin-induced diabetes and 3 healthy controls. The effect of two oligosaccharides – xylo- and galactooligosaccharides, and of aerobic training on the blood glucose concentration, growth and diversity of the gut microbiota was evaluated in the current study. Results: The galactooligosaccharides positively affected the glycemic status of the experimental animals as the diabetic and healthy rats had lower blood glucose concentration after 6 weeks of treatment (diabetic rats: week 4 vs. week 8, p=0.047; healthy rats: week 2,4,6,10 vs. week 8, p=0.001, p=0.000, p=0.025 and p=0.001, respectively). A positive effect of the galactooligosaccharides on body weight was observed when administered to diabetic rats in comparison to the diabetic control (p=0.020). Similar results were observed for the aerobically trained diabetic rats (p=0.004). The identification of bacterial species showed preserved microbiota diversity and indicated Bifidobacterium indicum , Lactobacillus feritoshensis and E. coli as the most abundant species among the analyzed genera. Conclusions: Prebiotic treatment beneficially affected the hyperglycemia and growth of type 1 diabetic rats. The most significant effect of the aerobic training was the improvement of the morphological parameters. Oligosaccharide administration and exercise did not affect the diversity of the bacterial species.

Introduction: Obesity is defined as chronic low-grade inflammation which is manifestation of the cellular response to a variety of stressful situations leading to organ and tissue damage. А high lipid diet could be assumed to be the trigger mechanism for the development of inflammatory processes leading to a disorder in the immune tolerance in the testis. Aim: The present study aimed at demonstrating the expression of inflammatory markers in the testis by a model of a high lipid diet and the possible effect on spermatogenesis. Materials and methods: Male Wistar rats were used in the study divided into two groups: a control group fed standard rodent food and an experimental group receiving high lipid food for 14 weeks. Routine histological techniques, immunohistochemical reactions for proinflammatory markers and morphometric analysis were performed to examine the testis preparations. Results: The high lipid diet caused a low-grade inflammation in the testis in the experimental group, which was confirmed by the increase of proinflammatory markers: the C-reactive protein, serum amyloid A, and interleukin-4, and by the elevated levels of angiotensin-converting enzyme in the experimental versus control groups in a rat experimental model. Conclusions: Our results suggest that a high lipid diet might be a possible cause for the idiopathic infertility in men.

Introduction: Sarcopenia, the progressive age-related decline in skeletal muscle mass, strength, and function, represents a major contributor to morbidity, frailty, and reduced quality of life in older adults. Oxidative stress and chronic low-grade inflammation are increasingly recognized as central mechanisms driving its onset and progression, through pathways involving mitochondrial dysfunction, impaired satellite cell activity, and dysregulated protein turnover. Objective: The purpose of the following manuscript is to summarize current research on the molecular and cellular interactions between oxidative stress and inflammation in sarcopenia, as well as to assess Aronia melanocarpa’s potential as a nutritional intervention. Methods: A narrative review was conducted by searching PubMed, Scopus, and Web of Science for peer-reviewed literature published between 2000 and 2024. Keywords included “sarcopenia”, “oxidative stress”, “inflammation”, “Aronia melanocarpa”, “polyphenols”, and even “functional foods”. Eligible publications provided mechanistic, preclinical, or clinical findings on skeletal muscle biology and A. melanocarpa bioactivity. Results: This narrative review examines the relationship between oxidative stress and inflammation in sarcopenia, focusing on NF-κB-mediated inflammatory signaling, Nrf-2-dependent antioxidant defenses, myokines like myostatin and irisin, and macrophage polarization in muscle homeostasis. Aronia melanocarpa (black chokeberry) is highlighted as a polyphenol-rich fruit with a distinct profile of anthocyanins and proanthocyanidins that have strong antioxidant and anti-inflammatory properties. According to preclinical, clinical, and nutritional studies, A. melanocarpa bioactives modulate redox balance, suppress pro-inflammatory cytokine production, increase antioxidant enzyme activity, and regulate metabolic and regenerative signaling pathways important for skeletal muscle health. Conclusions: Overall, the data suggest A. melanocarpa’s potential as a functional food and nutraceutical candidate for the prevention and treatment of sarcopenia. However, further translational and clinical research is needed to determine the appropriate intake, bioavailability, and long-term efficacy in human populations.

Background/Objectives: Boronic acid-based proteasome inhibitors (BABPIs) including Bortezomib, Ixazomib, and Delanzomib are clinically relevant anticancer agents whose mechanism of action depends on direct interaction between the boronic acid warhead and the threonine residue at the first position (Thr1), leading to the formation of covalent tetrahedral complex. Although the formation of this complex is well studied, the subsequent behavior of the boronic acid warhead, particularly the possible formation of monoanionic boronate species through deprotonation of one of the two boronic hydroxyl groups, remains unexplored. Therefore, the present study addresses whether the formation of Thr1-OH and a monoanionic boronate species is thermodynamically favorable and which of the two hydroxyl groups is more favorable for deprotonation. Methods: Density Functional Theory (DFT) calculations at the B3LYP/6-311+G(d,p) level, combined with the Polarizable Continuum Model (PCM), were used to study two competing deprotonation pathways for the inhibitors and for a simplified warhead model. To mimic the proteasome environment, reactions were modeled in different polar media—diethyl ether (ε = 4), methanol (ε = 33), and water (ε = 78). Results: Our DFT calculations confirmed that the covalent tetrahedral complex could convert into Thr1-OH and a monoanionic boronate species, representing the deprotonation of one of the boronic hydroxyl groups. Deprotonation via pathway 1 is more favorable than deprotonation via pathway 2 for all inhibitors, especially in polar solvents. Bortezomib demonstrated a strong preference for -OH₁ deprotonation with ∆∆G ≈ −7 kcal·mol⁻¹. In contrast, Ixazomib, Delanzomib, and the simplified warhead model showed smaller ∆∆G values (≈−2 kcal·mol⁻¹), within the method’s uncertainty (±2 kcal·mol⁻¹), suggesting both deprotonation modes under physiological conditions. Conclusions: These results provide comparative thermodynamic insight into the deprotonation behavior of BABPIs, suggesting that the two hydroxyl groups are not equivalent during deprotonation. This finding offers a physicochemical framework that may support the rational design of next-generation BABPIs.