Search Results (207)

Background and Objectives: In recent years, there has been growing interest in the production of ingredients rich in dietary fiber and antioxidants, such as green banana flours. This study evaluated the effect of consumption of mixed green banana pulp (PF) and peel (PeF) flours on the body weight gain, adiposity, lipid profile, and intestinal morphology of Wistar rats. Methods: Male young rats were divided into four groups (n = 8) that received a standard diet (SD), or one of the following three test diets: M1 (SD + 90% PF/10% PeF), M2 (SD + 80% PF/20% PeF), or P (SD + 100% PF) for 28 days. Results: Rats from M1, M2, and P groups showed reduced body weight gain and adiposity and had lower contents of total cholesterol, LDL-c, VLDL-c, and triglycerides. Animals from M1 and M2 groups had an increase in cecum weight, fecal moisture, acetic acid concentration, and crypt depth and reduced fecal pH. Moreover, consumption of the M1, M2, and P diets increased the expression of proteins involved in intestinal functionality. Significant negative correlations were observed between consumption of resistant starch and soluble dietary fiber, from the flours, and weight gain (r = −0.538 and r = −0.538, respectively), body adiposity (r = −0.780 and r = −0.767, respectively), total cholesterol (r = −0.789 and r = −0.800, respectively), and triglycerides (r = −0.790 and r = −0.786, respectively). Conclusions: Mixed green banana pulp and peel flour proved to be a viable alternative as a food ingredient that can promote weight loss, improve lipid profile and intestinal morphology, and minimize post-harvest losses. Full article

Background: Childhood obesity is a significant global health concern. Butyrylcholinesterase (BChE) has been shown to play a role in lipid metabolism. This study aimed to assess BChE activity, obesity-related and lipid-related indices, and dyslipidemia in obese and non-obese children, and to investigate the associations of these parameters with obesity among Thai children. Methods: The study included 661 Thai children, consisting of 338 with obesity and 323 with a normal weight. Anthropometric measurements, metabolic parameters, obesity- and lipid-related indices, and BChE activity were evaluated. Results: The obese group exhibited significantly higher BChE activity and obesity-related and lipid-related indices compared to the non-obese group (p < 0.01). Additionally, metabolic parameters—including glucose levels, triglyceride-glucose (TyG) index, and TyG-related indices—as well as the lipid profile, which included triglycerides (TG), non-high-density lipoprotein cholesterol (non-HDL-C), and very-low-density lipoprotein cholesterol (VLDL-C), were all significantly elevated in the obese group (p < 0.01). Obesity was associated with dyslipidemia (p < 0.01). Moreover, BChE activity showed a positive correlation with obesity-related and lipid-related indices, along with several metabolic parameters (p < 0.002). The upper stratum of BChE activity (OR = 5.356), the non-HDL-C/HDL-C ratio (OR = 2.185), and the TG/HDL-C ratio (OR = 1.703) were found to be effective in evaluating and predicting the risk of obesity, even after adjusting for potential covariates (p < 0.01). Conclusions: These findings indicate a significant relationship between obesity and increased BChE activity, lipid-related indices, and dyslipidemia in Thai children. Therefore, changes in BChE activity may be considered a factor associated with obesity, enhancing its potential as a marker for obesity assessment. Full article

Background/Objectives: Omega-3 highly unsaturated fatty acids (HUFAs), particularly EPA and DHA, have anti-inflammatory and lipid-modulating properties for treating atherosclerosis. However, the relationship between plasma fatty acid profiles, omega-3 status, and statin efficacy in carotid atherosclerosis remains poorly defined. Objectives: This study evaluates plasma and plaque fatty acid (FA) composition, explores their associations with plaque stability, and examines the relationship of omega-3 levels, lipid biomarkers (VLDL-C, LDL-C, HDL-C, total cholesterol, and triglycerides) with statin and β-blocker treatment. A mathematical model was developed to predict the erythrocyte omega-3 index from plasma. Methods: In this case–control study, plasma and carotid plaques of 52 patients undergoing carotid endarterectomy were analyzed. Plasma was compared with that of 50 healthy controls. FAs were quantified by LC-MS/MS. Plaques were histologically classified as stable or unstable. Results: Atherosclerotic patients showed disturbed FA metabolism, including decreased plasma omega-3 EPA + DHA, SFAs and HUFAs, increased MUFAs, and impaired desaturase and elongase activity. Unstable plaques had higher MUFA and lower HUFA content compared with stable plaques. Significant correlations between plasma EPA + DHA and HDL-C and triglycerides were observed in statin-naïve patients, whereas statins appeared to attenuate these associations. Co-treatment with β-blockers had no significant effect. A validated logit-based model accurately predicted the erythrocyte omega-3 index from plasma (R² = 0.782). Conclusions: Altered plasma and plaque FA profiles correlate with atherosclerosis’s plaque instability and inflammatory lipid profiles. Statins significantly influence these associations, suggesting their complex interaction with lipid metabolism. Plasma measurements of omega-3 fatty acids in combination with predictive modelling may be beneficial for diagnostic and therapeutic monitoring in carotid atherosclerosis. Full article

Background and Objectives: Over the past few decades, a substantial body of evidence has linked periodontitis to systemic diseases—including hypertension—but the mechanisms underlying this association are not fully understood. This study aims to identify the factors that may mediate this relationship, including an analysis of the inflammatory biomarker NLRP3 and IL-1β levels in serum and saliva in patients with both diseases. Materials and Methods: This study included 108 individuals (mean age, 47.8 years, SD 12.8), 38.9% male and 61.1% female. The participants were divided into four groups: Group I—26 healthy participants; Group II—24 participants with periodontitis; Group III—26 participants with hypertension; and Group IV—32 participants with both periodontitis and hypertension. Clinical examinations were performed to diagnose hypertension and periodontitis, including a survey and blood tests in all patients. NLRP3 and IL-1β levels in serum and saliva were measured using ELISA. Results: Patients with periodontitis and hypertension were significantly older than those without these conditions (respectively, p < 0.001 and p < 0.001) and had more missing teeth (respectively, p < 0.001 and p = 0.037). Higher values were found in the periodontitis and hypertension group than in healthy individuals for VLDL (p = 0.001), triglycerides (p = 0.001), CRP (p = 0.003), WBC (p = 0.007), blood sugar (p = 0.002), total cholesterol (p = 0.003), and LDL (p = 0.010). Significantly higher levels of NLRP3 in saliva (p = 0.038) and serum (p = 0.021) were observed in patients with periodontitis than in those without periodontitis. Significant correlations were found between serum NLRP3 levels and the presence of hypertension (p = 0.001) and between saliva IL-1β levels and the presence of hypertension (p = 0.010). Serum NLRP3 levels demonstrated a predictive value for hypertension (AUC 0.693, 95% CI 0.590–0.796, and p = 0.001), with an established cutoff value of 0.68 ng/mL (sensitivity 0.623, specificity 0.630). Conclusions: The higher levels and correlations of pro-inflammatory markers in serum and saliva observed in patients with periodontitis and hypertension support the hypothesis of a relationship between these diseases, likely mediated by low-grade systemic inflammation. Full article

Dyslipidemia is a well-known risk factor in the development and progression of atherosclerosis. VLDL plays a crucial role in maintaining lipid homeostasis; however, even minor fluctuations in its production, intracellular trafficking, and secretion can contribute to the progression of atherosclerosis. Fenofibrate is an FDA-approved drug that effectively lowers plasma triglycerides and VLDL-associated cholesterol while simultaneously increasing HDL levels. Although fenofibrate is a known PPARα agonist with several proposed mechanisms for its lipid-altering effects, its impact on the intracellular trafficking of VLDL has not yet been investigated. We observed that treatment of HepG2 cells with 50 µM of fenofibrate resulted in a significant reduction in VLDL secretion, as evidenced by a significant decrease in the secretion of ³H-labeled TAG, fluorescent TAG, and ApoB100 protein into the media. Using confocal microscopy to monitor VLDL intracellular trafficking, we observed a distinct change in VLDL triglyceride localization, suggesting delayed transport through the endoplasmic reticulum and Golgi. An immunoblot analysis revealed a decrease in Sar1B protein expression, a key regulator of COPII protein recruitment, which is essential for VTV formation and intracellular VLDL trafficking, the rate-limiting step in VLDL secretion. Our data reveal a novel mechanism by which fenofibrate alters the lipid profile by interfering with intracellular VLDL trafficking in hepatocytes. Full article

Background: Cardiovascular disease remains the leading cause of death worldwide, and dyslipidemia is a critical, modifiable risk factor. Aim: We sought to evaluate the relationship between polymorphisms in CETP (rs3764261), APOA5 (rs662799), IL6 (rs1800796), and PON1 (Q192R) and lipid parameters, and to assess their contribution to dyslipidemia and overall cardiovascular risk in an urban cohort from Cauca, Colombia. Methods: In this cross-sectional observational study, 304 participants aged 40–69 years were enrolled. Clinical, anthropometric, and biochemical data were collected, and genotyping was performed for the four target polymorphisms. We used descriptive statistics to characterize the sample, non-parametric tests to compare lipid levels by genotype, and multivariable logistic regression to identify independent predictors of dyslipidemia. Results: Individuals with dyslipidemia exhibited significantly higher total cholesterol and VLDL levels, lower HDL levels, and an elevated Castelli II index compared with the non-dyslipidemia group. Although CETP genotype frequencies differed between groups, only the APOA5 rs662799 variant was significantly associated with increased VLDL levels, suggesting its potential role as a genetic biomarker of cardiovascular risk. Conclusions: Our findings underscore the interplay between metabolic factors and genetic variants in the pathogenesis of dyslipidemia. Notably, the APOA5 rs662799 polymorphism emerged as a key determinant of VLDL concentration, highlighting its promise for personalized cardiovascular risk stratification and management in this population. Full article

Background/Objectives: Vitamin D deficiency in children has been linked to various metabolic disturbances, including dyslipidemia, which contributes to cardiovascular risk. This study aims to investigate the relationship between vitamin D levels and lipid profiles in children. Methods: A cohort of 332 children with either normal vitamin D or diagnosed vitamin D deficiency was recruited. Serum vitamin D levels were measured, and lipid profiles, including total cholesterol, low-density lipoproteins (LDLs), high-density lipoproteins (HDLs), and triacylglycerols (TAGs), were assessed. The data were analyzed using statistical methods. Results: This study found that children with higher serum vitamin D concentrations had significantly lower TAG (p = 0.033) and very-low-density lipoprotein (VLDL) (p = 0.038) levels and higher HDL levels (p = 0.042), indicating a more favorable lipid profile compared to those with lower vitamin D levels. Conclusions: This study demonstrates that vitamin D deficiency can be associated with dyslipidemia in children. These findings suggest that vitamin D supplementation may be an effective strategy for managing dyslipidemia and reducing cardiovascular risk in pediatric populations. Further research is needed to determine the long-term effects and optimal dosing of vitamin D in this context. Full article

Background: Metabolic Dysfunction Associated Steatotic Liver Disease (MASLD) is the accumulation of fat in the liver without excessive alcohol consumption or other known liver diseases. MASLD is the most common liver disease in adolescents with obesity. The aims of this study were as follows: (i) to determine which index (waist circumference BMI, WHtR, VAI, METS-IR, METS-VF, HSI, FLI, or MetS_zscore) best explains the prevalence of MASLD in adolescents with obesity; (ii) to determine whether there was a specific index that was most strongly associated with MASLD; (iii) to assess which liver function indexes were most strongly correlated with MASLD. Methods: A total of 758 adolescents with severe obesity (BMI z-score > 2) admitted at the Division of Auxology, Istituto Auxologico Italiano, IRCCS, Piancavallo-Verbania for a 3-week multidisciplinary body weight reduction program were selected. Anthropometric parameters (stature, body mass, BMI, and waist and hip circumference) were collected, and body composition (lean and fat mass) was determined using the tetrapolar bioimpedance analysis (BIA) technique. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transferase (gamma GT), alkaline phosphatase (ALP), bilirubin, glucose, total cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein cholesterol (VLDL-C), triglycerides (TG), and C-reactive protein (CRP) were measured using standard techniques. MASLD was diagnosed based on abdominal ultrasound results. Results: WHtR (65.76%) was the most sensitive compared with other indexes. The HSI (AUC: 0.67 (0.63–0.71, 95% CI), p-value < 0.05) showed the best performance in predicting MASLD, with the threshold for having MASLD considered at 48.22. The indexes that showed the worst performance in predicting MASLD were the MetS z-score (AUC: 0.56 (0.52–0.60)) and the VAI (AUC: 0.57 (0.52–0.61)). ALT (OR: 2.92 (2.29–3.77); 95% CI) and AST (OR: 2.52 (2.03–3.20)) were the parameters with a stronger correlation with MASLD. Conclusions: The most sensitive index for diagnosing MASLD was the WHtR, based exclusively on anthropometric parameters. HSI was the index that correlated the most with MASLD, while the parameters of liver function (ALT and AST) were the most strongly correlated with the disease and its severity. Full article

Diabetes mellitus is a chronic, degenerative, and multifactorial disease characterized by hyperglycemia, and at least 537 million people suffered from diabetes in 2021. Agave durangensis Gentry, a species of agave native to the state of Durango, reports phenolic compounds, flavonols, flavonoids, and saponins and could be an alternative for the treatment of diabetes. The aim of this work was to identify the compounds in the leaves of Agave durangensis Gentry and their potential activity in diabetes. The leaf extract of Agave durangensis Gentry (EAD) was characterized by ultra-performance liquid chromatography–mass spectrometry (UPLC-MS), and different families of bioactive compounds were quantified by analytical methods. Probable pharmacological targets were identified in silico, and the inhibition of dipeptidyl peptidase-4 (DPP4) was validated in vitro. A model of hyperglycemia was established with streptozotocin in male Wistar rats, and we administered EAD intragastrically at a dose of 300 mg/kg, as well as combinations of the extract with metformin and sitagliptin over 30 days. Biochemical and histological parameters were analyzed. We identified thirty-six major compounds, where triterpenes represented 30% of the extract. Molecular docking showed that the extract could interact with α-glucosidases and DPP4 since a large number of compounds in the extract have a Δ G lower than that reported for the controls, and DPP4 inhibition was confirmed by in vitro assays. In vivo assays demonstrated that the administration of the extract was able to significantly decrease glucose levels by 56.75% and glycosylated hemoglobin by 52.28%, which is higher than that reported for sitagliptin with a decrease of 35.22%. In addition, the extract decreased triglycerides by 59.28% and very-low-density lipoprotein (VLDL) cholesterol by 60.27%, and when administered in combination with metformin, it decreased them more than when metformin was administered alone. For all the above reasons, Agave durangensis Gentry extract could be used for the development of phytomedicine for the treatment of diabetes. Full article

There is growing evidence linking growth differentiation factor 15 (GDF15) to both metabolic dysfunction-associated steatotic liver disease (MASLD) and cardiovascular (CV) risk. Nevertheless, the potential relationship between circulating levels of GDF15 and key features of MASLD being predisposed to atherosclerotic CV disease is not fully unveiled. The aim of this study was to deepen into the role of circulating GDF15 levels on metabolic-associated liver injury and atherosclerotic CV disease. We determined the serum GDF15 levels in 156 participants of a metabolic patient-based cohort, and cross-sectionally explored its associations with liver injury and an advanced atherosclerotic lipoprotein profile assessed by nuclear magnetic resonance (¹H-NMR). Additionally, we prospectively evaluated the association between GDF15 levels at baseline and incident atherosclerotic CV disease after a 10-year follow-up. GDF15 was related to liver injury and inflammatory hallmarks, and it increased the likelihood for liver steatosis independently of confounding factors. Likewise, GDF15 was positively associated with an atherogenic profile, particularly with the number of very-low-density lipoproteins (VLDL) particles and its cholesterol and triglyceride content, and with an indicator of subclinical atherosclerosis (i.e., carotid intima–media thickness (cIMT)). The baseline serum GDF15 levels were higher in the patients with atherosclerotic CV disease (10.6%) after a 10-year follow-up than in the individuals without CV disease. Altogether, this study provides new insights into the role of GDF15 in both MASLD and CV disease. Full article

Background: Cytochrome P450 2B6 (CYP2B6) is a sexually dimorphic, anti-obesity CYP enzyme responsible for the metabolism of xeno- and endobiotics, including the metabolism of polyunsaturated fatty acids (PUFAs) into 9-hydroxyoctadecadienoic acid (9-HODE) and 9-hydroxyoctadecatrienoic acid (9-HOTrE). However, humanized CYP2B6 transgenic (hCYP2B6-Tg) mice are sensitive to diet-induced hepatic steatosis despite their resistance to obesity. The purpose of this study was to determine if 9-HODE, 9-HOTrE, or other factors contribute to the sexually dimorphic steatosis observed in hCYP2B6-Tg mice. Results: Cyp2b9/10/13-null (Cyp2b-null) mice were injected with either 9-HODE or 9-HOTrE for 2 days and were then subjected to a fasting period of 20 h to induce steatosis. Serum lipids were moderately increased, especially in females, after 9-HODE (triglycerides (TGs), very low-density lipoproteins (VLDLs)) and 9-HOTrE (high-density lipoproteins (HDLs), low-density lipoproteins (LDLs), cholesterol) treatment. No change in hepatic lipids and few changes in hepatic gene expression were observed in mice treated with either oxylipin, suggesting that these oxylipins had minimal to moderate effects. Therefore, to further investigate CYP2B6’s role in steatosis, hCYP2B6-Tg and Cyp2b-null mice were subjected to a 20 h fast and compared. Both male and female hCYP2B6-Tg mice exhibited increased steatosis compared to Cyp2b-null mice. Serum cholesterol, triglycerides, HDLs, and VLDLs were increased in hCYP2B6-Tg males. Serum triglycerides and VLDLs were decreased in hCYP2B6-Tg females, suggesting the greater hepatic retention of lipids in females. Hepatic oxylipin profiles revealed eight perturbed oxylipins in female hCYP2B6-Tg mice and only one in males when compared to Cyp2b-null mice. RNA-seq also demonstrated greater effects in females in terms of the number of genes and gene ontology (GO) terms perturbed. There were only a few overlapping GO terms between sexes, and lipid metabolic processes were enriched in hCYP2B6-Tg male mice but were repressed in hCYP2B6-Tg females compared to Cyp2b-nulls. Conclusions: hCYP2B6-Tg mice are sensitive to fasting-mediated steatosis in males and females, although the responses are different. In addition, the oxylipins 9-HODE and 9-HOTrE are unlikely to be the primary cause of CYP2B6’s pro-steatotic effects. Full article

Background/Objectives: This research investigated the effects of myricitrin on hypercholesterolemia and non-alcoholic fatty liver disease (NAFLD) in mice given a high-cholesterol diet (HCD). Methods: C57BL/6J mice were maintained for 20 weeks on an HCD with or without myricitrin. Results: Myricitrin had no impact on the food consumption, body weight, or plasma triglyceride concentrations. However, myricitrin-supplemented mice had lower plasma total cholesterol (TC) concentrations and LDL + VLDL-cholesterol/TC proportion, and higher HDL-cholesterol/TC proportion than control mice, which resulted in a markedly decreased atherogenic index. Moreover, the levels of plasma C-reactive protein, oxidized LDL, lipoprotein(a), and plasminogen activator inhibitor-1, which are indicators for cardiovascular disease (CVD), were reduced, while levels of plasma paraoxonase, a cardioprotective enzyme, were greater in myricitrin-supplemented mice than in control mice. Myricitrin also meaningfully reduced liver weight and hepatic cholesterol content, and slightly alleviated fatty liver and fibrosis caused by an HCD. The plasma and hepatic cholesterol-lowering effects of myricitrin were partly associated with decreased activities of hepatic 3-hydroxy-3-methylglutaryl-CoA reductase and acyl-CoA:cholesterol acyltransferase, which are involved in cholesterol synthesis and esterification, respectively, as well as mRNA expression. Myricitrin also altered other hepatic genes implicated in cholesterol homeostasis, including the downregulation of SREBP2 and ABCA1 mRNA expression and the upregulation of LDLR mRNA expression. Moreover, myricitrin decreased TBARS levels in the liver and erythrocytes by activating antioxidant enzymes (SOD and catalase). Conclusions: These results indicate that dietary myricitrin may offer therapeutic benefits for HCD-caused hypercholesterolemia and NAFLD, and may help reduce CVD risk. Full article

Background: Recently, we reported that longer-term mixed nut intake significantly reduced serum total and low-density lipoprotein (LDL)-cholesterol, but these markers may not fully capture lipoprotein-related cardiovascular disease (CVD) risk. Objectives: This randomized, controlled, single-blinded, crossover trial in older adults with overweight or obesity examined the effects of longer-term mixed nut consumption on lipoprotein particle size, number, and lipid distribution. Methods: Twenty-eight participants (aged 65 ± 3 years; BMI 27.9 ± 2.3 kg/m²) completed two 16-week periods (control [no nuts] vs. mixed nuts (60 g/day: 15 g of walnuts, pistachios, cashews, and hazelnuts), separated by an 8-week washout. Plasma lipoprotein particle numbers, sizes, and lipid distributions across subclasses were analyzed using high-throughput nuclear magnetic resonance (NMR) spectroscopy. Results: Mixed nut consumption significantly reduced Apolipoprotein B (ApoB) concentrations (−0.07 g/L; p = 0.009), total cholesterol (−0.27 mmol/L; p = 0.047), non-HDL cholesterol (−0.28 mmol/L; p = 0.022), and total triacylglycerol (TAG) (−0.27 mmol/L; p = 0.008). Total very large-density lipoprotein (VLDL) particle numbers decreased by 24 nmol/L (p < 0.001), with reductions observed across all VLDL subclasses. Total LDL particle numbers (p = 0.044), specifically intermediate-density lipoprotein (IDL) (p = 0.002) and large LDL particles (p = 0.015), were also reduced, while HDL particle numbers and sizes were unaffected. The mixed nut intervention significantly reduced cholesterol concentrations across all VLDL subclasses and IDL (all p < 0.01), with no changes in LDL or HDL subclasses. TAG concentrations showed reductions across all lipoprotein subclasses (all p < 0.05). Conclusions: Longer-term mixed nut consumption may lower CVD risk in older adults and favorable shifts in apoB-containing lipoprotein subclasses towards a less atherogenic profile. Full article

Background: Brassica nigra possesses a significant concentration of bioactive compounds and has been demonstrated to have a variety of pharmacological properties, although its sprout has not been extensively studied. Thus, the protective effects of Brassica nigra sprout hydroalcoholic extract (BNSE) on lipid homeostasis, hepatotoxicity, and nephrotoxicity in cyclophosphamide (CYP)-induced toxicity in rats were examined in this study. Methods: Four experimental rat groups (n = 8 for each group) were examined as follows: NR, normal rats that received normal saline by oral gavage daily; CYP, injected with a single dose of CYP at 250 mg kg⁻¹ intraperitoneally (i.p.) and did not receive any treatment, receiving only normal saline by oral gavage daily; CYP + BNSE250, injected with a single dose of CYP at 250 mg kg⁻¹ i.p. and treated with BNSE at 250 mg kg⁻¹ by oral gavage daily for three weeks; and CYP + BNSE500, injected with a single dose of CYP at 250 mg kg⁻¹ i.p. and treated with BNSE at 500 mg kg⁻¹ by oral gavage daily for three weeks. Results: The results indicated a significant increase (p < 0.05) in triglyceride (TG), cholesterol (CHO), low-density lipoprotein cholesterol (LDL-c), and very low-density lipoprotein cholesterol (VLDL-c) levels in CYP-induced toxicity rats. The administration of BNSE at 250 and 500 mg kg⁻¹ significantly (p < 0.05) attenuated TG, CHO, LDL-c, and VLDL-c at values comparable with the NR group. The most efficient treatment for improving the lipid profile and atherogenicity complication was BNSE at 500 mg kg⁻¹, performing even better than 250 mg kg⁻¹. Administrating BNSE at 250 or 500 mg kg⁻¹ improved the liver’s function in a dose-dependent manner. Comparing the lower dose of 250 mg kg⁻¹ of BNSE with 500 mg kg⁻¹ showed that administrating 250 mg kg⁻¹ attenuated alanine transaminase (ALT) by 28.92%, against 33.36% when 500 mg kg⁻¹ was given. A similar trend was observed in aspartate aminotransferase (AST), where 19.44% was recorded for BNSE at 250 mg kg⁻¹ and 34.93% for BNSE at 500 mg kg⁻¹. Higher efficiency was noticed for BNSE at 250 and 500 mg kg⁻¹ regarding alkaline phosphatase (ALP). An improvement of 38.73% for BNSE at 500 mg kg⁻¹ was shown. The best treatment was BNSE at 500 mg kg⁻¹, as it markedly improved liver function, such as total bilirubin (T.B.), in a dose-dependent manner. The administration of BNSE attenuated the total protein (T.P.), albumin, and globulin levels to be close to or higher than the typical values in NR rats. Conclusions: BNSE might be used for its promising hypolipidemic, hepatoprotective, and nephroprotective potential and to prevent diseases related to oxidative stress. Further research on its application in humans is highly recommended. Full article

From a detailed review of 90 experimental and clinical metabolomic investigations of obesity and metabolic dysfunction-associated steatotic liver disease (MASLD), we have developed metabolomic hallmarks for both obesity and MASLD. Obesity studies were conducted in mice, rats, and humans, with consensus biomarker groups in plasma/serum being essential and nonessential amino acids, energy metabolites, gut microbiota metabolites, acylcarnitines and lysophosphatidylcholines (LPC), which formed the basis of the six metabolomic hallmarks of obesity. Additionally, mice and rats shared elevated cholesterol, humans and rats shared elevated fatty acids, and humans and mice shared elevated VLDL/LDL, bile acids and phosphatidylcholines (PC). MASLD metabolomic studies had been performed in mice, rats, hamsters, cows, geese, blunt snout breams, zebrafish, and humans, with the biomarker groups in agreement between experimental and clinical investigations being energy metabolites, essential and nonessential amino acids, fatty acids, and bile acids, which lay the foundation of the five metabolomic hallmarks of MASLD. Furthermore, the experimental group had higher LPC/PC and cholesteryl esters, and the clinical group had elevated acylcarnitines, lysophosphatidylethanolamines/phosphatidylethanolamines (LPE/PE), triglycerides/diglycerides, and gut microbiota metabolites. These metabolomic hallmarks aid in the understanding of the metabolic role played by obesity in MASLD development, inform mechanistic studies into underlying disease pathogenesis, and are critical for new metabolite-inspired therapies. Full article