Improve Lipid Metabolism Research Articles

Efficacy of fish oil supplementation on metabolic dysfunction-associated steatotic liver disease: a meta-analysis

ObjectiveGlobally, the occurrence of Metabolic dysfunction-associated steatotic liver disease (MASLD) is on a steady rise. Fish oil has anti-inflammatory effects and can improve lipid metabolism. The article aims to assess the impact of fish oil supplementation on MASLD.MethodsWe conducted a systematic search of Cochrane, Embase, PubMed, and Web of Science up to September 31, 2024, for randomized control trials (RCTs). The risk of bias of the included RCTs was evaluated using the Cochrane Collaboration’s tool. Outcomes measured were aspects of liver injury, lipid profile, insulin resistance, anthropometric measurements, and more.ResultsSeven randomized controlled trials (RCTs) involving 439 participants were incorporated into the analysis. In general, the risk of bias in these RCTs was either low or not clearly defined. Pooled analysis showed that triglycerides [TG, pooled standard mean difference (SMD): −0.40 (95% CI: −0.58 to −0.21)], aspartate transaminase [AST, SMD: −0.29 (95% CI: −0.48 to −0.10)], HOMA-IR [SMD: −2.06 (95% CI: −3.36 to −0.49)] and waist circumference [Waist-C, SMD: −0.31 (95% CI: −0.54 to −0.08)] were significantly improved. But showed no significant benefits on alanine transaminase [ALT, SMD: −0.15 (95% CI: −0.45 to 0.15)], gamma-glutamyl transpeptidase [GGT, SMD: −0.07 (95% CI: −0.26 to 0.12)], body mass index [BMI, SMD: 0.16 (95% CI: −0.34 to 0.02)], high-density lipoprotein cholesterol [HDL, SMD: 0.02 (95% CI: −0.18 to 0.22)], low-density lipoprotein cholesterol [LDL, SMD: −0.01 (95% CI: −0.20 to 0.18)], Total Cholesterol [TC, SMD: −0.34 (95% CI: −0.70 to 0.01)] and so on.ConclusionThe current evidence supports the fish oil supplementation in improving MASLD. Fish oil supplementation may also regulate blood lipids and improve glucose metabolism disorders.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/#myprospero, identifier CRD42024513246.

Exploring Gender Differences in the Effects of Diet and Physical Activity on Metabolic Parameters.

Gender differences in metabolic response to lifestyle interventions remain poorly explored. This study aimed to evaluate the impact of a six-month Mediterranean diet (MD) intervention combined with regular physical activity on metabolic parameters in overweight adults. A prospective cohort study was conducted in an obesity clinic in Rome, Italy, involving overweight adults (BMI ≥ 25 kg/m2) motivated to improve their lifestyle. Participants (n = 205; 107 men and 98 women) self-selected into physical activity groups (aerobic, anaerobic, combined or no activity). Gender-specific metabolic changes were assessed, including lipid profiles, liver markers and fasting glucose. Significant gender differences in metabolic results were observed. Men showed greater reductions in total cholesterol (TC) and LDL, as well as significant reductions in alanine aminotransferase (ALT). Women showed a significant increase in HDL cholesterol. Fasting blood glucose decreased significantly in both sexes, with no differences between the sexes. Activity-specific analysis revealed that anaerobic activity significantly improved lipid metabolism in men, while aerobic activity produced the greatest benefits in women, including increased HDL and improved liver marker profiles. Therapeutic strategies combining MD and physical activity must take into account gender-specific physiological differences and the type of sport activity to optimise metabolic benefits. Personalised approaches may improve the management of cardiovascular risk factors in overweight individuals. This study is registered on ClinicalTrials.gov (NCT06661330).

Olivetol's Effects on Metabolic State and Gut Microbiota Functionality in Mouse Models of Alimentary Obesity, Diabetes Mellitus Type 1 and 2, and Hypercholesterolemia.

Disorders of glucose and lipid metabolism, such as obesity, diabetes mellitus, or hypercholesterolemia, can cause serious complications, reduce quality of life, and lead to increased premature mortality. Olivetol, a natural compound, could be proposed as a promising therapeutic agent for preventing, treating, or alleviating metabolic complications of such pathological conditions. In this study, the researchers conducted a broad parallel investigation of olivetol's effects on metabolic state and gut microbiota functionality in mouse models of alimentary obesity, diabetes mellitus type 1 and 2, and hypercholesterolemia. According to the results of the study, olivetol caused a lowering of body weight in C57Bl6 mice fed a high-fat diet and in ldlr(-/-) mice, decreased serum glucose levels in db/db mice, improved lipid metabolism in ldlr(-/-) mice, and prevented inflammatory infiltration of the pancreas and loss of insulin secretion in NOD mice. In addition, olivetol affected the composition and functional activity of gut microbiota communities, inducing an expansion of probiotic species such as Akkermansia muciniphila and Bacteroides acidifaciens and depleting the representation of pathobionts such as Prevotella, although olivetol supplementation did not influence the diversity or richness of the communities. These results suggest that olivetol is a promising therapeutic agent for preventing, treating, or alleviating the metabolic complications of obesity, diabetes mellitus type 1 and 2, and hypercholesterolemia; however, more investigations are required in order to attain a full understanding of its physiological effects.

Strawberry dietary intervention influences diversity and increases abundances of SCFA-producing bacteria in healthy elderly people.

The gut microbiome is amenable to dietary interventions, and polyphenol-rich diets have been shown to enhance abundances of bacteria associated with short-chain fatty acid (SCFA) production. We examined the effects of a strawberry-based intervention on the gut microbiome of 69 healthy elderly German adults. Participants in five groups consumed varying amounts of strawberries, freeze-dried strawberries, and capers in olive oil over 10 weeks as part of a randomized controlled trial. 16S rRNA sequencing was used to analyze differences in microbial composition, diversity, phenotypes, differential abundance, and functional pathways. The intervention group featuring the highest amounts of fresh and freeze-dried strawberries without capers in olive oil (group 4) showed changes in gut microbial diversity and differential abundance that could be linked to improved health. Beta diversity, based on weighted UniFrac distances, increased significantly (P = 0.0035), potentially pathogenic bacteria decreased (P = 0.04), and abundances of SCFA-producing genera Faecalibacterium and Prevotella increased significantly. Other findings included a significant reduction of CAG-352, Preveotellaceae_NK3B31-group, and Eubacterium coprostanoligenes (group 2), and a trend of lowered Firmicutes-to-Bacteroidetes ratio (P = 0.067) and a reduction in Ruminococcaceae (group 3). Our findings suggest that a dietary intervention based on strawberries can positively alter the gut microbiota of healthy elderly people as seen in an enrichment of SCFA-producing genera, increased diversity, and a reduction in potentially pathogenic bacteria.IMPORTANCEAging is often associated with changes in the gut microbiome, including a decline in beneficial bacteria and an increase in potentially pathogenic species. Addressing these changes through lifestyle interventions is of significant interest. Our study demonstrates that a 10-week dietary intervention with strawberries can beneficially modulate gut microbial composition and diversity in healthy elderly individuals. Notably, the group consuming the highest amount of strawberries (without capers in olive oil) initially had higher abundances of potentially pathogenic bacteria. Here, the intervention led to increased abundances of the beneficial genera Faecalibacterium and Prevotella, which are linked to health benefits including reduced inflammation and improved lipid metabolism. These findings suggest that strawberry consumption can positively influence gut microbial composition, thereby contributing to overall health and disease prevention in older adults.

Effects of hawthorn pectin and its oligomers on gut microbiota and metabolites in high-fat diet mice.

Pectin is an acidic heteropolysaccharide with natural, green, and inexpensive characteristics. Compared to polysaccharides, oligosaccharides are more easily utilized by the body, and the physiological function of hawthorn pectin oligosaccharides (POS) may vary depending on their degree of polymerization (DP). Therefore, we mainly studied the effects of hawthorn pectin (HP) and POS with different DP on gut microbiota disorders induced by high-fat diet (HFD). HP and POS both improved weight gain, dyslipidemia, and glucose homeostasis caused by HFD, and increased serum GLP-1 levels. Meanwhile, the increased expression of Gcg and Pcsk1 genes in the ileum of the treatment group further confirmed this result. In addition, HP and POS reduced certain opportunistic pathogens, while restoring the richness and diversity of the gut microbiota. Meanwhile, HP and POS can improve intestinal barrier dysfunction by increasing the claudin-1, occludin, ZO-1, and MUC2 genes. Furthermore, fecal metabolomics suggests that POS may enhance linoleic acid synthesis and improve lipid metabolism by upregulating 9,10-DHOME ((12Z)-9,10-dihydroxyoctadec-12-enoic acid), while HP cannot. Overall, the research results indicate that both HP and POS can improve the weight phenotype changes, gut microbiota disruption, and metabolites changes caused by HFD. Particularly, POS has a better effect than HP, and there are differences in the improvement effect of POS with different DP, among which POS with DP 5 has the most significant improvement effect. This discovery enhances a deeper comprehension of the biological activity of different POS, providing an important basis for further optimizing the application of POS as a functional food.

Probiotic interventions with highly acid-tolerant Levilactobacillus brevis strains improve lipid metabolism and gut microbial balance in obese mice.

Many studies have shown that specific lactic acid bacteria (LAB) strains can delay obesity, offering a viable alternative to medications and surgeries. However, the mining and development of highly effective LAB strains for obesity control is still limited. In this study, the naturally highly acid-tolerant and gamma-aminobutyric acid-producing Levilactobacillus brevis D17 and its glnR deletion strain were used to investigate their anti-obesity effects. In an 8-week mouse experiment, L. brevis D17 and its glnR-deletion strain D17ΔglnR significantly reduced weight gain by 28.4% and 29.1%, respectively, improving abnormal serum indicators and glucose metabolism caused by a high-fat diet. Furthermore, L. brevis D17 and its glnR-deletion strain D17ΔglnR successfully colonized in the gut. Both D17 and D17ΔglnR interventions significantly restored the relative abundance of Muribaculaceae, Ileibacterium valens, Lactobacillus, Faecalibaculum, Bifidobacterium globosum, Akkermansia muciniphila, and Romboutsia ilealis, whereas they significantly reduced potentially harmful bacteria like Leptogranulimonas, Flintibacter, and Alistipes. Additionally, L. brevis intervention effectively decreased the levels of primary bile acids and increased secondary bile acids in the gut, thus balancing bile acid metabolism. The transcriptional analysis suggested that D17 and D17ΔglnR interventions may activate the AMPK signaling pathway in the liver to inhibit lipogenesis, activate the cAMP pathway to promote lipolysis, and inhibit pro-inflammatory macrophage infiltration to block inflammatory responses. These results indicate that L. brevis D17 and its glnR-deletion mutant strain D17ΔglnR show great potential in combating obesity. Moreover, these results also provide insights into the underlying mechanism behind their anti-obesity properties.

Healthy Lifestyle and Metabolic Dysfunction-Associated Steatotic Liver Disease: A Study of the Efficacy of Fatty Liver Regression.

Obesity is the primary cause of metabolic dysfunction-associated steatotic liver disease (MASLD). Healthy lifestyle management has potential value in the treatment of MASLD. A total of 150 patients with MASLD diagnosed at the Health Management Center of our hospital were enrolled and randomly divided into a traditional treatment (control group, n = 75) and a healthy lifestyle group (observation group, n = 75). All patients underwent a 3-month intervention. Data on general information, body composition, glucose metabolism, lipid metabolism, and inflammatory factors were analyzed. The difference in the change in fatty liver grade was statistically significant ( P < 0.05). There were statistically significant differences in treatment efficiency for physical conditions ( P < 0.05), including body fat mass, body mass index, body weight, waist circumference, and waist-to-hip ratio. In addition, there were statistically significant differences in treatment efficiency for scales such as the Diet Rating Scale, Emotional Stress Scale, and Global Physical Activity Questionnaire ( P < 0.05). Differences in treatment efficiency for body fat parameters, including percentage of body fat, visceral fat area, aspartate aminotransferase, and diastolic blood pressure, were also statistically significant ( P < 0.05). After treatment, statistically significant differences were observed in interferon-γ, insulin, low-density lipoprotein cholesterol, triglycerides, and tumor necrosis factor-α ( P < 0.05). Our study indicates that a healthy lifestyle can effectively promote the reduction of fatty liver grade in patients with MASLD, demonstrating positive effects in improving lipid metabolism and inflammatory responses in these patients.

NXT629 Ameliorates Cholesterol Gallstones in Mice Model by Improving Lipid Metabolism Disorder and Cholesterol Homeostasis Through Inhibiting the GPAM Pathway.

NXT629, a PPAR-alpha antagonist, exerts widespread effects in many diseases; however, its function and relevant mechanism in cholesterol gallstones (CG) remain largely unknown. Male C57BL/6J mice were fed a regular diet or lithogenic diet (LD), followed by treatment with intraperitoneal injection of NXT629. H&E staining was performed to analyze hepatic pathological changes, and Oil red O staining was conducted to detect lipid accumulation. Concentrations of total cholesterol (TC), triglyceride (TG), phospholipids (PL), total bile acids (TBA), and cholesterol saturation index (CSI) in both bile and serum were analyzed using commercially available kits. The mRNA expressions of ABCG5/8, CYP7A1, CYP7B1, PPAR-α, and ABCB11 in mouse liver tissues were measured by qRT-PCR assay. Overexpression of glycerol-3-phosphate acyltransferase mitochondrial (GPAM) was constructed to investigate the molecular mechanism of NXT629 in CG. NXT629 could prevent the formation of cholesterol gallstones (CG) and improve lipid metabolic disorders in mice fed a lithogenic diet (LD). Treatment with NXT629 significantly reduced the levels of ABCG5, ABCG8, and ABCB11, while increasing the levels of CYP7A1 and CYP7B1 in the LD group. Additionally, NXT629 treatment downregulated GPAM expression in hepatic tissue from LD-fed mice. Overexpression of GPAM partially counteracted the beneficial effects of NXT629 on CG formation, lipid metabolic disorders, and lipid-related gene expressions. NXT629 can inhibit CG formation, improve lipid metabolism disorders and cholesterol homeostasisby inhibiting GPAM expression, suggesting that NXT629 may serve as a potential therapeutic strategy for cholesterol stones prevention and treatment.

Effects of Dietary Schizochytrium Algae as ω-3 PUFA Source on the Egg-Laying Quail Performance, Serum Indexes, and Egg Yolk Fatty Acids Contents.

The objective of this experiment is to investigate the effects of SAP or SAO as ω-3 PUFA raw materials on production performance, egg quality, serum immunity, serum lipids, and fatty acid deposition patterns in the eggs of laying quails. Chinese yellow-feathered quails served as the experimental subjects. A single-factor design was employed to randomly assign 1288 quails into four treatment groups, with seven replicates per treatment and 46 birds in each replicate. The groups included a control group (basal diet with no SAP), 1.6% SAP, 3.2% SAP, and 0.8% SAP + 0.3% SAO. The results indicate that: (1) Compared to the control group, the 0.8% SAP + 0.3% SAO group exhibited a reduction in daily egg-laying rate and egg mass, alongside an increased FCR; (2) the 3.2% SAP group enhanced egg yolk color, while the 1.6% SAP group reduced eggshell thickness, and the 0.8% SAP + 0.3% SAO group increased eggshell thickness; (3) compared to the control group, the 3.2% SAP group decreased total cholesterol (TC) and high-density lipoprotein cholesterol (HDL-C) levels in serum; the addition of either the 3.2% SAP or the 0.8% SAP + 0.3% SAO group significantly elevated quail serum immunoglobulin M (IgM) levels (p < 0.05); (4) in comparison to the control group, the addition of SAP or with SAP increased the contents of monounsaturated fatty acids (MUFA), polyunsaturated fatty acids (PUFA), docosahexaenoic acid (DHA), and ω-3 PUFA in 56-day-old egg yolks while reducing the ω-6/ω-3 ratio (p < 0.05). These findings suggest that SAP as a source of ω-3 PUFA raw materials could improve quail health by improving lipid metabolism and immunity. 3.2% SAP was recommended as the optimal level to produce the enriched ω-3 PUFA quail eggs with the ω-3 PUFA ≥ 300 mg/100 g.

Mechanistic insights into Y-Box binding protein-1 mediated regulation of lipid metabolism and oxidative stress in NAFLD via INHBE/TNF-β pathway

Nonalcoholic fatty liver disease (NAFLD) is a prevalent liver disorder that has emerged as a significant public health concern. This study aimed to investigate the mechanisms by which Y-box binding protein-1 (YB1) knockdown influences lipid metabolism and oxidative stress in palmitic acid (PA)-induced NAFLD LO2 cells. The expression of YB1 was analyzed using the GSE89632 dataset from the Gene Expression Omnibus (GEO) database. RNA sequencing was performed, followed by Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, and protein-protein interaction (PPI) network analyses to identify differentially expressed genes (DEGs). Quantitative Real-Time PCR (QRT-PCR), Western blotting, flow cytometry, and various biochemical assays were used to evaluate gene expression, lipid accumulation, and oxidative stress. Our results demonstrated that YB1 is highly expressed in NAFLD. RNA sequencing revealed 798 DEGs between the shCtrl and shYB1 groups, with 190 genes upregulated and 608 genes downregulated. Notably, we observed an increase in INHBE (Inhibin Beta E) expression, while EGR1, GDF15, NUPR1, and FOSB were decreased in NAFLD LO2 cells. YB1 knockdown, particularly when combined with INHBE suppression, significantly enhanced cell viability, improved lipid metabolism, and reduced reactive oxygen species (ROS) accumulation and malondialdehyde (MDA) content. The downstream mechanism was primarily associated with TNF-β signaling. Specifically, we observed decreased levels of TGF-β1, p-Smad2, and p-Smad3 following YB1 and INHBE knockdown. Furthermore, INHBE overexpression reversed the beneficial effects induced by YB1 knockdown. In conclusion, YB1 knockdown improves lipid metabolism and reduces oxidative stress in NAFLD LO2 cells, largely through the INHBE/TNF-β signaling pathway. These findings provide valuable insights into novel therapeutic strategies for managing NAFLD.

Study on the Mechanism of Bifidobacterium animalis subsp. lactis F1-3-2 Regulating Bile Acid Metabolism Through TMA-TMAO Pathway to Improve Atherosclerosis.

Atherosclerosis is a major cause of cardiovascular disease (CVD). The trimethylamine (TMA)-trimethylamine N-oxide (TMAO) pathway is a key crossover pathway highly associated with diet, gut microbiome, and atherosclerosis. The Bifidobacterium animalis subsp. lactis F1-3-2 (Bif. animalis F1-3-2, No. CCTCCM2020832) was screened through in vitro and in vivo experiments in the early stage of this study with excellent lipid-lowering and anti-inflammatory function. By building an atherosclerosis model and focusing on TMAO, the specific mechanism of Bif. animalis F1-3-2 to improve atherosclerosis was explored. The study found that Bif. animalis F1-3-2 effectively improved the accumulation of aortic plaque in atherosclerotic mice. The strain improved lipid metabolism in serum and liver. It decreased the serum TMA and TMAO, regulated bile acid composition, participated in the farnesoid X receptor (FXR) pathway to improve lipid metabolism, and further reduced the aortic macrophage foam cell accumulation. In addition, the strain could improve the structure of the intestinal microbiome and reduce the proportion of Firmicutes and Bacteroidetes. The abundance of Turicibacter, Clostridium sensu stricto_1, and Romboutsia was reduced at the genus level. The differential microbiota is highly correlated with bile acid metabolism, which is speculated to be involved in ameliorating atherosclerotic lipid metabolism disorders.

Z-Ligustilide: A Potential Therapeutic Agent for Atherosclerosis Complicating Cerebrovascular Disease.

Atherosclerosis (AS) is one of the major catalysts of ischemic cerebrovascular disease, and the death and disease burden from AS and its cerebrovascular complications are increasing. Z-ligustilide (Z-LIG) is a key active ingredient in Angelica sinensis (Oliv.) Diels and Ligusticum chuanxiong Hort. In this paper, we first introduced LIG's physicochemical properties and pharmacokinetics. Then, we reviewed Z-LIG's intervention and therapeutic mechanisms on AS and its cerebrovascular complications. The mechanisms of Z-LIG intervention in AS include improving lipid metabolism, antioxidant and anti-inflammatory effects, protecting vascular endothelium, and inhibiting vascular endothelial fibrosis, pathological thickening, and plaque calcification. In ischemic cerebrovascular diseases complicated by AS, Z-LIG exerts practical neuroprotective effects in ischemic stroke (IS), transient ischemic attack (TIA), and vascular dementia (VaD) through anti-neuroinflammatory, anti-oxidation, anti-neuronal apoptosis, protection of the blood-brain barrier, promotion of mitochondrial division and angiogenesis, improvement of cholinergic activity, inhibition of astrocyte proliferation, and endoplasmic reticulum stress. This paper aims to provide a basis for subsequent studies of Z-LIG in the prevention and treatment of AS and its cerebrovascular complications and, thus, to promote the development of interventional drugs for AS.

Exploring the Potential Advantages of Chocolate and Cocoa for Cardio and Cerebrovascular Health

Numerous studies have identified cocoa phenolics, procyanidins, and flavan-3-ols as bioactive antioxidant compounds that enhance vascular function, reduce inflammation, and improve lipid metabolism, insulin sensitivity, and platelet aggregation. Research indicates that consuming flavanol-rich cocoa supports cardiovascular health. Given the rising global occurrence of cardiovascular disease and its related risk factors, this review article aimed to investigate the impact of chocolate/cocoa intake on cardio and cerebrovascular conditions and their related risks. Across various clinical trials, moderate flavonol-rich cocoa/chocolate consumption proved to be correlated with better heart health. Advantages include a diminished risk of heart failure, hypertension, platelet aggregation, coronary artery disease, stroke, atrial fibrillation, high cholesterol, and peripheral artery disease. Consuming 50 grams of dark chocolate daily or every other day has been linked to these positive outcomes. While flavanol-rich chocolate shows potential as a complementary therapy for various cardio and cerebrovascular conditions, extensive clinical trials are necessary to confirm its effectiveness.

Medium chain triglycerides alleviate non-alcoholic fatty liver disease through bile acid-mediated FXR signaling pathway: A comparative study with common vegetable edible oils.

With the global epidemic trend of obesity, non-alcoholic fatty liver disease (NAFLD) has become a significant cause of chronic liver disease, seriously affecting human health. Medium-chain triglycerides (MCT) with a fatty acid chain length varying between 6 and 10 carbon atoms (most sources from coconut and palm kernel oils), which exhibited activities to improve lipid metabolism, prevent cardiovascular diseases, and enhance immunity. However, the efficacy differences and potential mechanisms between MCT and traditional long-chain vegetable oils (palm oil, PA; high oleic peanut oil, OA) in obesity-induced NAFLD were still unclear. The present study treated obesity-induced NAFLD mice with different dietary lipids for 16weeks. The results showed that MCT supplements significantly improved abnormal elevation of weight gain and blood lipids and reduced hepatic lipid accumulation to a greater extent than PA and OA. Furthermore, bile acid profiling results indicated that MCT significantly changed the composition of bile acids in the liver, reduced the concentrations of cholic acid (CA), deoxycholic acid (DCA), β-muricholic acid (β-MCA), and ursodeoxycholic acid (UDCA) and increased the concentrations of chenodeoxycholic Acid (CDCA), taurochenodeoxycholic acid （TCDCA), hyodeoxycholic acid (HDCA), and taurohyodeoxycholic acid (THDCA). Mechanistically, MCT supplement upregulated FXR signal and inhibited the expression of key genes for triglyceride synthesis in the liver, thereby reducing hepatic lipid accumulation. In summary, MCT exerted a superior effect on PA and OA in improving obesity-induced NAFLD. These results provided new evidence for the application of MCT in treating NAFLD.

Unlocking the Potential: How Flavonoids Affect Angiogenesis, Oxidative Stress, Inflammation, Proliferation, Invasion, and Alter Receptor Interactions in Endometriosis.

Endometriosis, though not classified as a carcinogenic condition, shares features such as oxidative stress, migration, invasion, angiogenesis, and inflammation with tumor cells. This study aims to review the effects of flavonoids on these processes and their molecular mechanisms in preventing and treating endometriosis. A comprehensive review was conducted, involving a literature search in online databases using keywords like "endometriosis," "endometrioma," and "flavonoid." Two authors screened the literature based on predefined criteria, and the selected studies were summarized in a structured data extraction table. Studies reviewed showed that various flavonoids impact key processes in endometriosis, including angiogenesis, inflammation, oxidative stress, and invasiveness. Flavonoids such as 2',7'-dichlorodihydrofluorescein diacetate (H2DCF-DA), naringenin, apigenin, myricetin, 5,7-dimethoxyflavone (DMF), chrysin, and 6,8-diprenylorobol were found to induce oxidative stress. Xanthohumol, isoliquiritigenin, and luteolin demonstrated effects on angiogenesis. Apigenin, isoliquiritigenin, and luteolin exhibited anti-inflammatory properties. Additionally, 3,6-dihydroxyflavone, isoliquiritigenin, and naringenin displayed anti-invasive activities. Flavonoid-receptor interactions further enhance their therapeutic potential in endometriosis management. Flavonoids such as nobiletin, chrysin, and daidzein modulate PPARγ and PPARα, reducing inflammation, promoting apoptosis, and improving lipid metabolism. These interactions regulate critical pathways in angiogenesis and immune responses. Additionally, flavonoids impact the aryl hydrocarbon receptor (AhR), with compounds like resveratrol inhibiting cell proliferation and cholesterol biosynthesis, further suppressing lesion growth. The ability of flavonoids like quercetin and kaempferol to antagonize NR4A1 leads to reduced cell proliferation and oxidative stress in endometriotic tissues. These findings offer insights into the mechanisms through which specific flavonoids modulate angiogenesis, inflammation, oxidative stress, and invasiveness in endometriosis. By targeting receptors such as PPARs, AhR, and NR4A1, flavonoids demonstrate the capacity to modulate both metabolic and inflammatory pathways, offering a multifaceted approach to managing endometriosis. Flavonoids can selectively target pathophysiologic molecules and pathways implicated in the condition. Consequently, leveraging the therapeutic attributes of flavonoids could lead to novel strategies for managing endometriosis.

A charge reversal nano-assembly prevents hepatic steatosis by resolving inflammation and improving lipid metabolism

Lipid metabolism imbalance combined with over-activated inflammation are two key factors for hepatic stestosis. However, on-demand anchoring inflammation and lipid metabolism disorder for hepatic stestosis treatment has yet to be realized. Here we propose a charge reversal fullerene based nano-assembly to migrate hepatic steatosis via inhibiting macrophage-mediated inflammation and normalizing hepatocellular lipid metabolism in obesity mice. Our nano-assembly (abbreviated as FPPD) is comprised of electropositive polyetherimide (PEI), charge-shielded dimethylmaleic anhydride (DMA), and poly(lactic-co-glycolic acid) (PLGA), which provides hydrophobic chains for self-assembly with anti-oxidative dicarboxy fullerene poly(ethylene glycol) molecule (FP). The obtained FPPD nano-assembly owns a charge reversal ability that switches to a positive charge in an acidic environment that targets the electronegative mitochondria both in pro-inflammatory macrophages and steatosis hepatocytes. We demonstrate that the anti-oxidative and mitochondria-targeting FPPD notably reduces inflammation in macrophages and lipid accumulation in hepatocytes by quenching excessive reactive oxygen species (ROS) and improving mitochondrial function in vitro. Importantly, FPPD nano-assembly reveals a superior anti-hepatic steatosis effect via migrating inflammation and facilitating lipid transport in obesity mice. Overall, the charge reversal nano-assembly reduces over-activated inflammation and promotes lipid metabolism that provides an effectiveness of a multi-target strategy for hepatic steatosis treatment.

Multimodal prehabilitation to improve functional abilities and reduce the chronic inflammatory response of frail elderly patients with gastric cancer: A prospective cohort study.

Population ageing and cancer burden are important global public health problems that pose unprecedented threats to health systems worldwide. Frailty is a common health problem among elderly patients with cancer. In recent years, the use of prehabilitation to improve frailty has received widespread attention. Few studies have addressed the specific physiologic effects of prehabilitation on patients undergoing surgery. Frail elderly patients (aged at least 65 years) who underwent elective primary surgery for gastric cancer between September 2022 and October 2023 were included in this single-centre prospective cohort study and were categorized into multimodal prehabilitation or ERAS standard care groups. Prehabilitation, including physical and respiratory training, nutritional support and psychosocial treatment, was provided at least two weeks before gastrectomy. The primary outcome was functional status. Secondary outcomes included changes in indices of lipid metabolism, oxidative stress and chronic inflammation. Over a 13-month period, 137 participants were assessed for eligibility, and 110 patients (prehabilitation 55, ERAS 55) were analysed. Compared with the baseline, patients in the prehabilitation group exhibited increased physical capacity before the operation (mean 6-min walk test change +28m; P<0.001). After prehabilitation intervention, inflammation-related indicators (NLR, PLR, SII and CRP) improved, and proinflammatory cytokine production (IL-5, IL-6, IL-1β, IL-10 and TNF-α) decreased. After surgery, the increase in IL-6 was reduced in the prehabilitation group (P=0.036). Moreover, prehabilitation was associated with alleviating oxidative stress as determined by the levels of MDA (P=0.005). Multimodal prehabilitation can play a beneficial role in improving functional abilities by reducing chronic inflammation, improving lipid metabolism, and attenuating oxidative stress.

The Beneficial Effects of Curcumin on Lipids: Possible Effects on Dyslipidemia-induced Cardiovascular Complications.

Dyslipidemia and altered lipid metabolism are closely involved in the pathogenesis and clinical manifestation of many metabolic and non-metabolic diseases. Therefore, mitigation of pharmacological and nutritional factors together with lifestyle modifications is paramount. One potential nutraceutical exhibiting cell signaling and lipid-modulating properties implicated in dyslipidemias is curcumin. Specifically, recent evidence suggest that curcumin may improve lipid metabolism and prevent dyslipidemia-induced cardiovascular complications via several pathways. Although the exact molecular mechanisms involved are not well understood, the evidence presented in this review suggests that curcumin can provide significant lipid benefits via modulation of adipogenesis and lipolysis, and prevention or reduction of lipid peroxidation and lipotoxicity via different molecular pathways. Curcumin can also improve the lipid profile and reduce dyslipidemia- dependent cardiovascular problems by impacting important mechanisms of fatty acid oxidation, lipid absorption, and cholesterol metabolism. Although only limited direct supporting evidence is available, in this review we assess the available knowledge regarding the possible nutraceutical effects of curcumin on lipid homeostasis and its possible impacts on dyslipidemic cardiovascular events from a mechanistic viewpoint.

Methionine and vitamin E supplementation improve production performance, antioxidant potential, and liver health in aged laying hens

Sulfur metabolites of methionine (Met) and vitamin E (VE) have antioxidant potential and can maintain liver health in chickens. This study explored the underlying mechanisms of Met sources, the ratio of total sulfur amino acids to lysine (TSAA: Lys), and VE levels on production performances, antioxidant potential, and hepatic oxidation in aged laying hens. Eight hundred and sixty-four, Hy-Line Brown laying hens (70-week age) were divided into 12 treatment groups, each having 6 repeats and 12 birds/each repeat. The dietary treatments consisted of DL-Met (DL-Met), DL-2-hydroxy-4-(methylthio)-butanoic acid (OH-Met), 3 ratios of TSAA: Lys (0.90, 0.95, and 1.00), and 2 levels of VE (20 and 40 g/ton). Albumen height and Haugh unit significantly increased at a lower level of VE (P < 0.05). Triglycerides (TG), total cholesterol (TC), low-density lipoprotein (LDL), and very low-density lipoprotein (VLDL) in serum and superoxide dismutase (SOD) and catalase activities (CAT) in the liver significantly reduced at 0.95 TSAA: Lys ratio (P < 0.05). Fatty acid synthase (FAS), lipoprotein lipase (LPL), nuclear factor erythroid 2-related factor 2 (Nrf2), and carnitine palmitoyltransferase-1 alpha (CPT-1α) also upregulated at this TSAA: Lys ratio (P < 0.05). Compared with the DL-Met group, the OH-Met group had lower Dipeptidyl Peptidase 4 (DPP4) and higher TC, LDL, and VLDL concentrations (P < 0.05).The expression of FAS,CPT-1α), glutathione (GSH), glutathione disulfide (GSSG), glutathione synthetase (GSS), and Nrf2 were significantly higher in OH-Met compared with the DL-Met group (P < 0.05). OH-Met at 0.95 and DL-Met at 0.90 TSAA: Lys ratio showed higher CAT and lower aspartate aminotransferase (AST) activities. Moreover, OH-Met at 0.90 and DL-Met at 0.95 of the TSAA: Lys ratio had a significant reduction of malondialdehyde (MDA) (P < 0.05). Overall, these results suggest that OH-Met source with a lower level of VE positively influenced production performance and improved liver health in aged laying hens through improved lipid metabolism and hepatic antioxidant function.

Structure characteristics of a novel pectic polysaccharide from Fructus Corni and its protective effect on alcoholic fatty liver.

Alcoholic fatty liver disease (AFLD) is characterized by the accumulation of hepatic lipid and has no effective treatment yet. Fructus Corni is a traditional Chinese medicinal herb, and its extractions have demonstrated hepatoprotective properties. We hypothesize that the polysaccharides in Fructus Corni might have therapeutic effects on AFLD. In this study, we isolated a novel homogeneous polysaccharide, APFC-2 (Mw=63.0kDa), from the Fructus Corni, and its structure was elucidated by monosaccharide composition, methylation analysis, partial acid hydrolysis, and NMR spectra. APFC-2 is a pectic polysaccharide characterized by a backbone of T-β-Galp-(1→6)-β-Galp-(1→3,6)-β-Galp-(1→[4)-α-GalpA-OMe-(1 →4)-α-GalpA-(1→]m→[2,4)-α-Rhap-(1→4)-α-GalpA-(1→]n, with branches comprising T-Araf-(1→, →3)-α-Araf-(1→, →3,5)-α-Araf-(1→, and →5)-α-Araf-(1→. In vivo experiments indicated that APFC-2 could significantly reduce hepatic steatosis, fasting triglyceride, and cholesterol levels in AFLD mice. Cell proliferation and Oil Red O staining results showed that APFC-2 concentration-dependently increased cell viability and significantly improved lipid metabolism in vitro. Mechanistically, APFC-2 markedly inhibited the formation of lipid both in vitro and in vivo through activating liver kinase B1 (LKB1) and then regulating adenosine 5'-monophosphate-activated protein kinase (AMPK)-SREBP-1 and AMPK-PPAR-α pathways. This research provides a theoretical basis for the potential application of Fructus Corni pectic polysaccharide as a specific activator of LKB1 for treating AFLD.