Introduction: Metabolic dysfunction-associated steatotic liver disease (MASLD) affects approximately one-third of the global population. Meanwhile, the development of MASLD is related to dysbiosis of the gut microbiota (GM). Our previous studies have shown that Vitamin K2 (VK2) has considerable potential to ameliorate mitochondrial dysfunction in mice fed a high-fat diet (HFD); however, the mechanism through which VK2 improves mitochondrial function and mitigates MASLD remains unclear.
Objective: This study aimed to elucidate the mechanism through which VK2 modulates MASLD.
Methods: A total of 80 C57BL/6J mice (4-5 weeks old) were fed a HFD for 16 weeks to establish the MASLD animal model. Additionally, VK2 was administered at a dose of 120 mg/kg/day for the last 8 weeks; 30 mice were fed a normal diet for the entire 24-week period. Mice were randomly divided into groups according to different experimental protocols. Hematoxylin and Eosin (H&E) staining, Oil Red O staining, and Cluster of Differentiation 11b (CD11b) immunofluorescence staining were used to detect liver histology and inflammatory cell infiltration in the mouse liver tissues. Moreover, 16S rRNA gene sequencing, antibiotic treatment, and fecal microbiota transplantation (FMT) were employed to investigate the microbiota-mediated anti-MASLD effects of VK2. Adeno-associated virus 9 (AAV9) was used to elucidate the mechanism through which VK2 regulates MASLD severity.
Results: VK2 significantly reduced hepatic lipid (triacylglycerol (TG) and total cholesterol (TC)) levels, as well as serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in HFD-fed mice (p < 0.05). VK2 also significantly suppressed inflammatory responses (p < 0.05), oxidative stress (p < 0.05), and improved mitochondrial dysfunction (p < 0.05) in a GM-dependent manner. Furthermore, VK2 restored the balance in the intestinal microbiota primarily through regulating Lactobacillus spp. abundance, and markedly alleviated MASLD via a GM-dependent manner. VK2 notably upregulated the expression of SIRT3 signaling pathway proteins (p < 0.05), thereby reducing MASLD-associated mitochondrial dysfunction (p < 0.05).
Conclusions: VK2 exerts promising therapeutic effects mainly through enhancing intestinal Lactobacillus abundance and ameliorating mitochondrial dysfunction.
Background: Prolonged or intense exercise can disrupt gastrointestinal (GI) function and gut microbiota, impairing athletic performance. Dietary fibre supplementation may enhance gut microbiota diversity, improve body composition, and promote recovery in athletes. This study aimed to explore the effects of dietary fibre supplementation at two doses for 8 weeks on these aspects in college basketball players.
Methods: Twenty male college basketball players (aged 17-25 years) were randomly assigned to a high-dose group (HDG; 10 participants; 6.84 g/day dietary fibre) or a low-dose group (LDG; 10 participants; 3.24 g/day dietary fibre). The participants consumed fibre-enriched meals daily while maintaining their regular training schedules. The outcome measures included gut microbiota diversity (metagenomic sequencing), body composition, fatigue recovery markers, glucose and lipid metabolism, and athletic performance. Statistical analyses included paired and independent t tests for within- and between-group comparisons and Spearman's correlation analysis to assess the relationships between gut microbiota and biochemical markers.
Results: One participant in the high-dose group withdrew, and nineteen ultimately completed the study. Both groups showed significant within-group improvements (p < 0.05) in body weight (HDG: -2.77 ± 0.76 kg; LDG: -2.40 ± 0.67 kg), body fat percentage (HDG: -1.87 ± 0.69; LDG: -1.49 ± 0.45), cortisol (HDG: -6.79 ± 4.26 μg/dL; LDG: -4.5 ± 4.84 μg/dL), maximum power (HDG: 27.16 ± 9.77 W; LDG: 14.50 ± 9.43 W), maximal oxygen uptake (HDG: 8.78 ± 0.97; LDG: 6.90 ± 1.37), and half-court triangle run times (HDG: -0.48 ± 0.36 s; LDG: -0.25 ± 0.20 s). Meanwhile, fasting blood glucose significantly decreased (0.91 ± 0.55 mmol/L; p = 0.001), and the gut microbiome changes were more stable in the HDG, whereas the LDG presented greater shifts in microbial diversity. No significant between-group differences were observed.
Conclusions: Dietary fibre supplementation improved the gut microbiome composition, body composition, fatigue recovery, and athletic performance of college basketball players, regardless of dosage. Further studies are needed to evaluate higher doses and specific fibre types.
Background: Retinol-binding protein 4 (RBP4) is a vitamin A transport protein synthesized in the liver and also plays a crucial role in inflammation and immune regulation. Low serum vitamin A levels have been observed in both pediatric and adult patients with ulcerative colitis (UC). The association between serum vitamin A levels and serum RBP4 levels, as well as the underlying mechanism involved inimpaired vitamin A transport during inflammation in UC patients, has yet to been investigated.
Methods: A validation cohort comprising 103 UC patients and 22 controls was analyzed. Serum RBP4 levels were measured using anenzyme-linked immunosorbent assay (ELISA), and correlations with vitamin A levels and disease severity wereassessed. A dextran sulfate sodium (DSS)-induced colitis mouse model was used to valuatehepatic RBP4 expression and inflammatory changes. Primary hepatocytes from C57BL/6 mice were exposed to inflammatory cytokines to assess the impact of these cytokines on RBP4 expression.
Results: Serum vitamin A (p < 0.001) and RBP4 levels (p < 0.001) were significantly lower in UC patients compared to controls, exhibiting a pronounced decreasing trend as disease severity increased (vitamin A: p < 0.001; RBP4: p < 0.001), while vitamin A levels increased after effective treatment (p < 0.001). Hepatic RBP4 expression was reduced in the DSS-induced colitis model and negatively correlated with TNF-α, IL-6, and IL-17.
Conclusions: Serum RBP4 levels are decreased in UC patients and negatively correlate with disease severity, possibly due to proinflammatory cytokine-induced suppression which might contribute to inflammation-driven vitamin A transport dysfunction.
Background: Dietary interventions have exhibited promise in restoring microbial balance in chronic kidney disease. A low-protein calorie-restricted diet can reduce kidney injury in diabetic rodents. However, whether the renoprotective effects of this dietary intervention in murine diabetic kidney disease models are linked to gut microbiota modulation remains to be determined.
Methods: Diabetic mice (induced by high-fat diet and streptozotocin) were randomized into four groups (n = 8/group): normal protein (20% protein), caloric restriction (30% restriction), low-protein (13% protein), and low-protein calorie-restricted (13% protein + 30% restriction). After a 5-week intervention, blood and urine samples were collected for relevant analyses, fecal samples for gut microbiota analysis, and kidney tissues for histological, immunohistochemical, and Western immunoblotting assays.
Results: The low-protein calorie-restricted diet significantly improved glycemic control (fasting blood glucose: p < 0.01), ameliorated dyslipidemia (all p < 0.01), and mitigated kidney damage in diabetic mice. Additionally, the low-protein calorie-restricted diet ameliorated gut microbiota dysbiosis, significantly suppressing the increase in Firmicutes/Bacteroidetes ratio (p = 0.02) and decreasing serum trimethylamine oxide levels (67.51 ± 1.47 ng/mL vs. 56.58 ± 5.75 ng/mL; p < 0.01). Compared to the normal protein group, the low-protein calorie-restricted group exhibited significant reductions in serum tumor necrosis factor-α (TNF-α) levels (20.75 ± 7.83 μmol/L vs. 5.37 ± 2.45 μmol/L; p < 0.01) and apoptosis-associated speck-like protein containing a CARD (ASC), NOD-like receptor family pyrin domain containing 3 (NLRP3), and interleukin-1β (IL-1β) expression in kidney tissue (all p < 0.01).
Conclusions: The low-protein calorie-restricted diet exerts renoprotective effects in mice with diabetic kidney disease, possibly by modulating the gut-kidney axis to reduce circulating trimethylamine oxide levels, suggesting a potential link to NLRP3 inflammasome suppression in kidney tissue.
Diabetes mellitus (DM) is a chronic metabolic disorder characterized by persistent hyperglycemia and associated with severe complications, including cardiovascular diseases, neuropathy, nephropathy, and retinopathy. Although synthetic antidiabetic drugs are available, the side effects and limited long-term effectiveness of these medications highlight the urgent need for safer, more potent alternative therapies. Ginkgo biloba L., a traditional medicinal plant rich in flavonoids, terpenoids, and bilobalide, has attracted attention for its potential role in diabetes management. This review critically evaluates the antidiabetic potential of G. biloba by analyzing evidence from in vitro, in vivo, and clinical studies. Moreover, this review highlights the pharmacological actions of G. biloba and its key bioactive compounds, focusing on their mechanisms of action, including the activation of adenosine monophosphate-activated protein kinase (AMPK), the translocation of glucose transporter type 4 (GLUT4), and the inhibition of protein tyrosine phosphatases. The review also discusses the therapeutic implications of G. biloba supplementation and identifies gaps in clinical validation, optimal dosing, and safety profiling. Preclinical studies have demonstrated that G. biloba improves glycemic control by enhancing glucose uptake, regulating insulin secretion, inhibiting α-glucosidase activity, and exerting antioxidant and anti-inflammatory effects. Additionally, clinical trials suggest that supplementation with G. biloba can reduce oxidative stress, improve lipid profiles, and mitigate diabetes-related complications. However, despite these promising outcomes, inconsistencies remain in present study designs, dosages, and patient populations, which question the validity of results. Furthermore, studies related to the antidiabetic effect and underlying mechanisms of G. biloba, such as modulation of AMPK pathways and GLUT4 expression, also remain inadequate and warrant further systematic investigation. G. biloba may still be considered a complementary treatment approach in managing diabetes due to its broad pharmacological activities and favorable safety profile. However, well-designed, large-scale clinical trials are crucial for establishing standardized dosing regimens, confirming long-term safety, and fully elucidating the mechanisms of action. Integrating G. biloba into therapeutic strategies could offer a natural, and effective adjunct for enhancing glycemic control and reducing diabetes-related complications.
The vitamin B complex, a group of water-soluble vitamins, is essential for various metabolic and cellular processes and critical for achieving optimal surgical outcomes in plastic and cosmetic procedures. This review examines the mechanistic contributions of this complex at the cellular level, including any roles in mitochondrial bioenergetics, redox balance, gene regulation, and cellular repair mechanisms. Niacinamide, as a precursor to NAD⁺, enhances mitochondrial efficiency and facilitates energy production, supporting tissue regeneration. Pyridoxine functions as a cofactor in neurotransmitter biosynthesis and amino acid metabolism, contributing to nerve recovery post-surgery. Furthermore, cobalamin is crucial for maintaining the myelin sheath and facilitating axonal repair, thereby ensuring neuronal integrity and minimizing nerve damage. Additionally, pantothenic acid, through its role in coenzyme A synthesis, regulates fatty acid metabolism and accelerates cellular repair, aiding in wound healing. Biotin is fundamental for keratin synthesis and follicular cell proliferation, promoting skin integrity and hair regeneration, which are vital in aesthetic and reconstructive treatments. Meanwhile, thiamine ensures a sufficient energy supply for neuronal recovery and cellular resilience through modulating carbohydrate metabolism. Thus, by integrating these cellular mechanisms, the vitamin B complex enhances tissue repair, minimizes inflammation, and improves both aesthetic and functional outcomes. Advances in precision supplementation, innovative drug delivery methods, and regenerative medicine continue to expand the therapeutic potential of B vitamins in plastic and reconstructive surgery. This comprehensive overview underscores the clinical significance of these vitamins in optimizing surgical recovery and promoting long-term tissue health.
Background: The effects of dietary niacin on the risk of cardiovascular disease (CVD) and mortality in patients with chronic kidney disease (CKD) remain unclear.
Methods: CKD patients with estimated glomerular filtration rates (eGFRs) 20-59 mL/min/1.73 m2 or urinary albumin/creatinine ratio ≥30 mg/g were identified in the National Health and Nutrition Examination Survey (NHANES) data from 2003 to 2018. Age, gender, race, education level, marital status, body mass index, blood pressure, and smoking and drinking history were considered as confounders.
Results: The present study encompassed 3815 CKD patients eligible for inclusion based on the study criteria. Participants with a niacin intake of >27.7 mg/d (quartile 4) had a lower prevalent CVD risk than those with an intake of ≤14.67 mg (quartile 1) (odds ratio (OR), 0.710, 95% CI: 0.560-0.900; p for trend = 0.004). In the follow-up with a median of 7.0 years, 323 from CVD. After adjustment, a higher niacin intake (>27.7 mg) reduced CVD mortality compared to a lower intake (≤14.67 mg) (hazard ratio (HR), 0.610, 95% CI: 0.480-0.770; p for trend <0.001). Adding dietary niacin to clinical variables increased the C-index from 0.746 to 0.749 for CVD prevalence and from 0.659 to 0.682 for mortality. The net reclassification improvement increased by 9.0% and 13.1% for CVD and mortality, respectively, and the integrated discrimination improvement increased by 0.3% and 1%, respectively.
Conclusions: Higher dietary niacin intake may reduce CVD and its mortality in individuals with CKD.
Background: Obesity, a prevalent global health issue, is associated with testosterone deficiency (TD). A body shape index (ABSI) provides a more precise assessment of obesity and visceral fat, but its relationship with testosterone remains unclear. This study aimed to explore the association between ABSI and testosterone levels leading to TD.
Methods: Data from 5256 adult males participating in the National Health and Nutrition Examination Survey (NHANES) from 2011 to 2016 were collected to analyze of the association between ABSI and TD. The data underwent analysis using multivariate linear regression, logistic regression, restricted cubic spline (RCS) analysis, subgroup analysis, and interaction testing. The predictive ability of ABSI based on weight, height, and waist circumference, as well as body mass index (BMI) based on weight and height, alongside a multiplicative combination of both metrics, BMI × ABSI, and optimal proportional combination OBMI + ABSI for assessing TD risk, was valuated using receiver operating characteristic (ROC) curves.
Results: Following adjustment for all confounding factors, ABSI exhibited a negative linear correlation with testosterone (β = -6.99, 95% confidence interval (CI): -8.25 to -5.73; p < 0.001) and a positive association with TD risk (odds ratio (OR) = 1.06, 95% CI: 1.04-1.08; p < 0.001). Notably, these associations remained consistent in the subgroup analysis. Additionally, age and hypertension demonstrated significant interactions between ABSI and TD (p < 0.05). Moreover, combining metrics, such as BMI × ABSI and OBMI + ABSI, proved to be more reliable predictors of TD compared to BMI or ABSI alone.
Conclusions: This study identified a negative linear correlation between ABSI and total testosterone levels in adult American males, as well as a positive linear correlation with TD prevalence. ABSI represents a valuable addition to BMI for assessing obesity and the association between obesity and TD.
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