Search Results (48)

Childhood obesity is a substantial health problem worldwide. The origin of obesity (increased adiposity) can be partly traced back to intrauterine life. However, the determinants of fetal fat deposition remain unclear. This study investigated the association between cord blood adipocytokines related to lipid metabolism (leptin, adiponectin, and insulin-like growth factor-1 [IGF-1]) and fetal adiposity during gestation. A prospective study was conducted in a cohort of 94 singleton pregnancies. Fetal ultrasonography was performed at 24, 30, and 36 weeks of gestation. Estimated fetal adiposity (EFA) was calculated by integrating measurements of cross-sectional arm and thigh fat area percentages and anterior abdominal wall thickness. Plasma cytokine levels and C-peptide immunoreactivity (as a proxy for fetal insulin resistance) were evaluated in cord blood samples obtained at delivery. The associations of cord blood leptin, adiponectin and IGF-1 levels with EFA at 24, 30, and 36 weeks were determined by multiple linear regression, adjusted for potential covariates. The multivariate analyses indicated that leptin was significantly correlated with EFA at 30 and 36 weeks. Leptin was also positively correlated with C-peptide immunoreactivity in the umbilical cord. Cord adiponectin levels were not associated with EFA across gestation. Cord IGF-1 levels were significantly correlated with EFA and estimated fetal body weight (EFW) at 36 weeks. In conclusion, cord leptin was associated with EFA at 30 and 36 weeks, and IGF-1 was associated with EFA at 36 and EFW at 36 weeks. In Conclusion, cord leptin was associated with EFA at 30 and 36 weeks, and IGF-1 was associated with EFA and EFW at 36 weeks. Considering the effects of leptin and IGF-1 on fetal insulin resistance and lipid metabolism, increased levels of leptin and IGF-1 are potential plasma biomarkers of increased fetal adiposity, which may predispose to infant obesity and metabolic dysfunction in later life. Full article

Microplastics (MPs) are contaminants of emerging concern, and the study of their effects on several species, especially freshwater organisms, has not been exhausted. Erpobdella johanssoni, a freshwater leech, was used as a model in this study for the assessment of the potentially toxic effects of polyethylene microplastics (PE-MPs) 40–48 µm in size under controlled laboratory conditions. PE-MP toxicity was assessed in the examined leech using four increasing concentrations (1, 10, 100, and 1000 µg/L) during an exposure period of 7 days. Oxidative damage was detected through the increase in malondialdehyde (MDA) levels, reflecting the occurrence of lipid peroxidation. The activities of enzymes involved in the antioxidant response, such as catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx), increased. Furthermore, the histopathology of the body wall, muscle cells, botryoidal cells, and ovaries was assessed to understand and evaluate the acute toxicity of PE-MPs. The histopathological changes detected in PE-MP-treated leeches varied in a concentration-dependent manner. Overall, this research indicated that even at environmentally relevant concentrations, PE-MPs had biological effects on the studied leeches and, consequently, on the freshwater invertebrate clade. This finding could provide novel insights into the effects of plastic pollution on freshwater ecosystems, particularly on invertebrate health and biodiversity. Full article

Objective: Various insulin resistance (IR) indices have been developed to assess cardiovascular (CVS) risk. We compared the association between ten IR indices and cardiac, renal, and vascular end-organ measures in a predominantly young (age 45.0 ± 18.3 years) South African Black population. Methods: We assessed the relationships between ten IR indices (homeostatic model assessment for IR [HOMA-IR], quantitative insulin sensitivity check index [QUICKI], metabolic score for IR [METS-IR], triglyceride–glucose index [TyG], TyG–body mass index [TyG-BMI], TyG–waist circumference [TyG-WC], TyG–waist-to-height ratio [TyG-WHtR], triglyceride to high-density cholesterol concentration [TyG-HDL], lipid accumulation product [LAP], visceral adiposity index [VAI]) and end-organ measures in 779 community participants of African ancestry. Results: HOMA-IR and QUICKI were the only IR indices consistently associated with end-organ measures (left ventricular [LV] mass index, p ≤ 0.005; LV relative wall thickness, p < 0.0001; early-to-late mitral velocity, p ≤ 0.01; E/e’, p ≤ 0.002; e’, p < 0.0001; pulse wave velocity, p = 0.036 (HOMA-IR only); glomerular filtration rate [GFR], p < 0.0001), independent of confounders. Furthermore, HOMA-IR was consistently higher, and QUICKI lower, in those with compared to those without end-organ damage (LV hypertrophy [p ≤ 0.03], concentric LV [p < 0.03], and reduced GFR [p ≤ 0.008]), independent of confounders. Importantly, the associations between HOMA-IR or QUICKI and end-organ measures were independent of additional CVS risk factors, including adiposity measures, and were replicated in the participants without diabetes mellitus (n = 669) and in the participants without high blood pressure (n = 505). Conclusions: In a predominantly young community of African ancestry, of ten recommended IR indices, only HOMA-IR and QUICKI were consistently associated with end-organ damage independent of CVS risk factors. Full article

Background: A growing body of evidence links a high-fructose diet (HFrD) to metabolic disturbances, including inflammation, dyslipidemia, insulin resistance and also endothelial dysfunction, yet its role in allergic asthma remains underexplored. Considering that obesity and hypercholesterolemia exacerbate asthma by promoting systemic inflammation, investigating interventions with dual metabolic and anti-inflammatory effects is essential. This study aimed to evaluate the potential modulatory effects of rosuvastatin in ameliorating the effects of HFrD-induced metabolic and vascular dysfunction in the context of allergic asthma. Methods: Forty-eight Sprague-Dawley rats were assigned to eight groups, receiving either a standard or HFrD for 12 weeks. Allergic asthma was induced using an ovalbumin sensitization and challenge protocol, while controls were administered saline. Selected groups were treated with rosuvastatin throughout the entire duration of the experiment. Body weight, abdominal circumference and serum biomarkers were assessed at baseline, 6 and 12 weeks. Endothelial function was assessed by evaluating vascular reactivity in an isolated organ bath. Additionally, histopathological analyses of aortic and pulmonary tissues were conducted to investigate inflammatory responses and morphological changes. Results: Rats on HFrDs exhibited significant increases in body weight, abdominal circumference, lipid profiles and blood glucose, which were further aggravated by allergic asthma. Rosuvastatin treatment notably reduced lipid levels, C-reactive protein and immunoglobulin E, while also enhancing vascular reactivity and attenuating aortic and bronchial wall thickening. Conclusions: Our findings suggest that rosuvastatin may serve as an effective therapeutic agent for addressing vascular and inflammatory complications associated with a high fructose intake and allergic asthma. Full article

Sulphated polysaccharides (SPs) are negatively charged compounds found in the cell wall of seaweeds or marine macro algae. These compounds exhibit a range of pharmacological activities, including anti-obesity effects. The aim of this systematic review as well as meta-analysis was to assess the potentials of seaweed-derived SPs to mitigate obesity through a systematic review and meta-analysis of animal model-based studies. A comprehensive summary of the included articles was conducted, focusing on the following obesity-related parameters: food intake, body weight gain, epididymal fat size, adipocyte size, liver weight, serum alanine transaminase (ALT) and aspartate transaminase (AST), insulin and tumour necrosis factor-α (TNF-α), and the lipid profile (total cholesterol, triglyceride, high-density lipoprotein cholesterol (HDL-c), and low-density lipoprotein cholesterol (LDL-c)). The systematic review demonstrated that seaweed-derived SPs exhibit ameliorative effects against obesity, as evidenced by reductions in food intake, body weight gain, epididymal fat and adipocyte size, liver weight, ALT and AST levels, serum insulin and TNF-α, LDL-c, total cholesterol, and triglycerides and an increase in HDL-c in obese rats administered with seaweed-derived SPs. However, the meta-analysis revealed statistically significant anti-obesity effects of seaweed-derived SPs for most, but not all the parameters tested. Further research in human subjects is necessary not only to ascertain the results of preclinical studies but also to provide conclusive evidence of the anti-obesity potential of SPs in humans. Full article

Background/Objectives: The rapidly increasing rate of obesity has become an extremely important public health problem, particularly in developed countries. Obesity is associated with a range of health problems, often referred to as the metabolic syndrome. Adipose tissue is now regarded as an endocrine organ responsible for the hormonal secretion of adipokines, which are cytokines involved in various physiological processes. It has been established that adipokines play a key role in the regulation of many processes in the human body. The aim of the current study was to use an animal model to investigate the possible influence of obesity and adipokines on the gestational period, on the development of offspring, and to assess whether these changes are influenced by the administration of antioxidant agents and flavonoids. Methods: The present study was performed using 5 groups of 7 female Wistar albino rats. A control group was used to which a 5% lipid diet was administered, and the other 4 groups were fed an obesogenic 65% lipid diet. From the 4 groups that received obesogenic diet one group received no supplement, and the rest of 3 received Detralex, Sel-E-Vit and Rutin (antioxidants and flavonoids). Study times for both pregnant groups and offsprings: on day 15 of gestation, venous blood was drawn to determine adipokine (leptin and visfatin) levels; on days 18–22 ultrasound examination was performed to measure the thickness of adipose tissue in the abdominal wall; for each batch a number of 10 offspring were selected for the measurements (pup weight, brain weight, head length, head width, spine length, width between shoulder blades, coxal bone length), adipokine levels in the offspring (from brain tissue) were also determined, as well as the existence of changes in the brain tissue of the offspring identified by electron microscopy. Results: The results of the study showed that the high-fat diet (HFD) led to a significant increase in body weight and abdominal wall thickness in pregnant females compared to the control group. The levels of leptin and visfatin were also affected by the HFD, with leptin levels being significantly higher in the HFD group and visfatin levels being lower. In the offspring, the HFD group had a significantly higher body mass and brain weight compared to the control group. The anthropometric measurements of the offspring were also affected by the maternal diet, with the HFD group having larger dimensions overall. Interestingly, the offspring of the groups that received flavonoids in addition to the HFD had significantly smaller dimensions compared to both the HFD group and the control group. Conclusions: The results of this experimental study reinforce what is already known about the effects of obesity on the gestation period and offspring and at the same time, the current study highlights the existence of possible adverse effects of flavonoid compounds on the development of pregnancy and offspring, opening the way for future studies on the benefits and risks of using these compounds during gestational period. Full article

Background/Objectives: In this paper, we created enteric delayed-release granules that load Dendrobine (DNL) directly into the intestinal flora of hyperlipidemic mice, based on the relationship between intestinal flora and hyperlipidemia. Methods: We then used pharmacodynamics and 16 Sr RNA high-throughput sequencing to examine the hypolipidemic effects and mechanism of these granules. Solvent evaporation was used to create the DNL, which was then characterized using FT–IR, XRD, SEM, and DSC. A high-fat diet was used to create the mouse model of hyperlipidemia in C57BL/6J mice. Dendrobine, various dosages of DNL, TMAO, and the combination of TMAO and DNL were subsequently gavaged on the mice. The makeup of the intestinal flora in the mouse colon was analyzed using 16S rRNA sequencing, and the effectiveness and mechanism of DNL in controlling the intestinal flora for the treatment of hyperlipidemia in mice were investigated. Results/Conclusions: The findings showed that DNL could effectively improve the dysbiosis brought on by hyperlipidemia by significantly lowering the mice’s body weight and blood lipid level (p < 0.05), while also regulating the function of their intestinal flora, increasing the abundance of Actinobacteria (p < 0.05) and Thick-walled bacterium (p < 0.05), and decreasing the abundance of Desulfovibrio (p < 0.05) and Mycobacterium anisopliae (p < 0.05) in the intestinal flora of mice, inhibiting the growth of intestinal harmful microorganisms, providing space for the reproduction of beneficial bacteria, and thus maintaining the stability of the intestinal flora’s structure. Full article

The general features of the shift to a dormant state in mycobacterial species include several phenotypic changes, reduced metabolic activities, and increased resistance to host and environmental stress conditions. In this study, we aimed to provide novel insights into the viability state and morphological changes in dormant M. smegmatis that contribute to its long-term survival under starvation or hypoxia. To this end, we conducted assays to evaluate cell viability, morphological changes and gene expression. During starvation, M. smegmatis exhibited a reduction in cell length, the presence of viable but non-culturable (VBNC) cells and the formation of anucleated small cells, potentially due to a phenomenon known as reductive cell division. Under hypoxia, a novel population of pleomorphic mycobacteria with a rough surface before the cells reached nonreplicating persistence 1 (NRP1) was identified. This population exhibited VBNC-like behaviour, with a loss of cell wall rigidity and the presence of lipid-body-like structures. Based on dosR and hspX expression, we suggest that M. smegmatis encounters reductive stress conditions during starvation, while lipid storage may induce oxidative stress during hypoxia. These insights into the heterogeneous populations presented here could offer valuable opportunities for developing new therapeutic strategies to control dormant mycobacterial populations. Full article

Extracellular vesicles (EVs) are vesicle-like structures composed of lipid bilayers, which can be divided into apoptotic bodies, microbubbles and exosomes. They are nanoparticles used for the exchange of information between cells. EVs contains many substances, including protein. With the development of proteomics, we know more about the types and functions of protein in vesicles. The potential functions of proteins in the envelope are mainly discussed, including cell wall construction, fungal virulence transmission, signal transmission and redox reactions, which provides a new perspective for studying the interaction mechanism between fungi and other organisms. The fungal protein markers of EVs are also summarized, which provided an exploration tool for studying the mechanism of vesicles. In addition, the possible role of immune protein in the EVs in the treatment of human diseases is also discussed, which provides new ideas for vaccine development. Full article

Chronic low-grade inflammation (CLGI) is associated with obesity and is one of its pathogenetic mechanisms. Lipopolysaccharide (LPS), a component of Gram-negative bacterial cell walls, is the principal cause of CLGI. Studies have found that capsaicin significantly reduces the relative abundance of LPS-producing bacteria. In the present study, TRPV1-knockout (TRPV1^−/−) C57BL/6J mice and the intestinal epithelial cell line Caco-2 (TRPV1^−/−) were used as models to determine the effect of capsaicin on CLGI and elucidate the mechanism by which it mediates weight loss in vivo and in vitro. We found that the intragastric administration of capsaicin significantly blunted increases in body weight, food intake, blood lipid, and blood glucose in TRPV1^−/− mice fed a high-fat diet, suggesting an anti-obesity effect of capsaicin. Capsaicin reduced LPS levels in the intestine by reducing the relative abundance of Proteobacteria such as Helicobacter, Desulfovibrio, and Sutterella. Toll-like receptor 4 (TLR4) levels decreased following decreases in LPS levels. Then, the local inflammation of the intestine was reduced by reducing the expression of tumor necrosis factor (TNF)-α and interleukin (IL)-6 mediated by TLR4. Attenuating local intestinal inflammation led to the increased expression of tight junction proteins zonula occludens 1 (ZO-1) and occludin and the restoration of the intestinal barrier function. Capsaicin increased the expression of ZO-1 and occludin at the transcriptional and translational levels, thereby increasing trans-endothelial electrical resistance and restoring intestinal barrier function. The restoration of intestinal barrier function decreases intestinal permeability, which reduces the concentration of LPS entering the circulation, and reduced endotoxemia leads to decreased serum concentrations of inflammatory cytokines such as TNF-α and IL-6, thereby attenuating CLGI. This study sheds light on the anti-obesity effect of capsaicin and its mechanism by reducing CLGI, increasing our understanding of the anti-obesity effects of capsaicin. It has been confirmed that capsaicin can stimulate the expression of intestinal transmembrane protein ZO-1 and cytoplasmic protein occludin, increase the trans-epithelial electrical resistance value, and repair intestinal barrier function. Full article

Abdominal aortic aneurysm (AAA) is a chronic aortic disease that lacks effective pharmacological therapies. This study was performed to determine the influence of treatment with the gasdermin D inhibitor necrosulfonamide on experimental AAAs. AAAs were induced in male apolipoprotein E-deficient mice by subcutaneous angiotensin II infusion (1000 ng/kg body weight/min), with daily administration of necrosulfonamide (5 mg/kg body weight) or vehicle starting 3 days prior to angiotensin II infusion for 30 days. Necrosulfonamide treatment remarkably suppressed AAA enlargement, as indicated by reduced suprarenal maximal external diameter and surface area, and lowered the incidence and reduced the severity of experimental AAAs. Histologically, necrosulfonamide treatment attenuated medial elastin breaks, smooth muscle cell depletion, and aortic wall collagen deposition. Macrophages, CD4⁺ T cells, CD8⁺ T cells, and neovessels were reduced in the aneurysmal aortas of necrosulfonamide- as compared to vehicle-treated angiotensin II-infused mice. Atherosclerosis and intimal macrophages were also substantially reduced in suprarenal aortas from angiotensin II-infused mice following necrosulfonamide treatment. Additionally, the levels of serum interleukin-1β and interleukin-18 were significantly lower in necrosulfonamide- than in vehicle-treated mice without affecting body weight gain, lipid levels, or blood pressure. Our findings indicate that necrosulfonamide reduced experimental AAAs by preserving aortic structural integrity as well as reducing mural leukocyte accumulation, neovessel formation, and systemic levels of interleukin-1β and interleukin-18. Thus, pharmacologically inhibiting gasdermin D activity may lead to the establishment of nonsurgical therapies for clinical AAA disease. Full article

Atherosclerosis (AS) is a chronic inflammatory disease of large- and medium-sized arteries that causes ischemic heart disease, strokes, and peripheral vascular disease, collectively called cardiovascular disease (CVD), and is the leading cause of CVD resulting in a high rate of mortality in the population. AS is pathological by plaque development, which is caused by lipid infiltration in the vessel wall, endothelial dysfunction, and chronic low-grade inflammation. Recently, more and more scholars have paid attention to the importance of intestinal microecological disorders in the occurrence and development of AS. Intestinal G-bacterial cell wall lipopolysaccharide (LPS) and bacterial metabolites, such as oxidized trimethylamine (TMAO) and short-chain fatty acids (SCFAs), are involved in the development of AS by affecting the inflammatory response, lipid metabolism, and blood pressure regulation of the body. Additionally, intestinal microecology promotes the progression of AS by interfering with the normal bile acid metabolism of the body. In this review, we summarize the research on the correlation between maintaining a dynamic balance of intestinal microecology and AS, which may be potentially helpful for the treatment of AS. Full article

This study aimed to investigate the effects of cyclosporine on the morphology, cell wall structure, and secretion characteristics of Cryptococcus neoformans. The minimum inhibitory concentration (MIC) of cyclosporine was found to be 2 µM (2.4 µg/mL) for the H99 strain. Yeast cells treated with cyclosporine at half the MIC showed altered morphology, including irregular shapes and elongated projections, without an effect on cell metabolism. Cyclosporine treatment resulted in an 18-fold increase in chitin and an 8-fold increase in lipid bodies, demonstrating changes in the fungal cell wall structure. Cyclosporine also reduced cell body and polysaccharide capsule diameters, with a significant reduction in urease secretion in C. neoformans cultures. Additionally, the study showed that cyclosporine increased the viscosity of secreted polysaccharides and reduced the electronegativity and conductance of cells. The findings suggest that cyclosporine has significant effects on C. neoformans morphology, cell wall structure, and secretion, which could have implications for the development of new antifungal agents. Full article

Nuts are high nutrient-dense foods containing healthy lipids, dietary fiber, and bioactive phytochemicals, including vitamins and minerals. Although the beneficial effect of nut consumption on different chronic diseases has been well documented, especially in relation to their cardiometabolic benefits, less scientific evidence is available on their possible beneficial effects on gastrointestinal health. In this narrative review, we summarize the most important findings and new research perspectives in relation to the importance of nut consumption on gastrointestinal health. The integrity of the cell wall structure, cell size and particle size after mastication are known to play a crucial role in energy, nutrient and bioactive release from nuts during digestion, therefore affecting bioaccessibility. Other mechanisms, such as cell wall composition, thickness and porosity, as well as stability of the membranes surrounding the oil bodies within the cell, are also important for energy extraction. As the undigested nutrients and phytochemicals are delivered to the colon, effects on gut microbiota composition are predicted. Although the overall effect of nut consumption on microbial alpha- and beta-diversity has been inconsistent, some scientific evidence suggests an increase in fecal butyrate after almond consumption, and a beneficial role of walnuts on the prevention of ulcerative colitis and protection against the development of gastric mucosal lesions. Full article

Obesity, currently defined as a disease, is associated with a number of metabolic disorders, and oxidative stress is discussed as the link between them. The aim of this study was to analyze the plasma markers reflecting oxidative modification of lipids and lipoproteins, oxidized LDL (oxLDL) and thiobarbituric acid reactive substances (TBARS), under the influence of the 75 g of oral glucose during oral glucose tolerance test (OGTT), in patients with increased body mass. One hundred twenty individuals of both genders (46 women and 74 men) aged 26 to 75 years with increased body mass (BMI > 25 kg/m²) were recruited for the study. OGTT was performed in each of the qualified persons, and glycemia, insulinemia, and concentrations of oxLDL and TBARS were measured fasting and at 120 min of OGTT. The homeostasis model assessment of insulin resistance (HOMA-IR) was used to assess the degree of insulin resistance (IR). In order to assess the changes of the investigated parameters under the influence of 75 g glucose, the index R_OGTT = [120’]/[0’] was calculated to obtain oxLDL-R_OGTT and TBARS-R_OGTT. The statistical analysis was performed in the entire study population and subsequent groups from H1 to H4, defined by HOMA-IR quartiles. In the entire study population and the subgroups, oxidative stress markers changed during OGTT. From H1 to H4 group, increasing oxLDL and TBARS were observed both in the fasting state and at 120 min of OGTT, and the oxLDL-R_OGTT index decreased from the H2 to the H4 group. The intensification of IR in people with increased body mass may predispose them to enhanced oxidative modification of lipoproteins. Individual reduction in the concentration of oxLDL during OGTT, in reference to fasting value (decreased oxLDL-R_OGTT), suggests increased uptake of modified lipoproteins by scavenger receptor-presenting cells or increased migration to the vascular wall. Full article