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.
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.
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.
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.
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.
This study aimed to elucidate the mechanism through which VK2 modulates MASLD.
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.
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).
VK2 exerts promising therapeutic effects mainly through enhancing intestinal Lactobacillus abundance and ameliorating mitochondrial dysfunction.
Polycystic ovary syndrome (PCOS) is a leading endocrine disorder in reproductive-aged women. While dietary interventions are widely advocated, the distinct roles of adiposity and dietary inflammation in driving PCOS phenotypes remain unclear. Therefore, this study aimed to dissect the contributions of body mass index (BMI) and dietary inflammatory index (DII) to hyperandrogenism and insulin resistance (IR) in PCOS.
This cross-sectional study included 115 women with PCOS who visited gynecology and infertility clinics affiliated with Tabriz University of Medical Sciences. Data from the DII were computed using a validated 168-item semi-quantitative food frequency questionnaire. The free androgen index (FAI) was calculated as follows: (total testosterone (nmol/L)/SHBG (nmol/L)) × 100. The relationships between the BMI and DII and FAI, the Homeostasis model assessment of insulin resistance (HOMA-IR), the Homeostasis model assessment of β-cell function (HOMA-β), the quantitative insulin sensitivity check index (QUICKI), sex hormone binding globulin (SHBG), testosterone, fasting insulin (FI), and fasting blood sugar (FBS) were assessed using descriptive and analytical statistics. The general linear model was applied to adjust for confounders.
The mean (standard deviation, SD) BMI and FAI among subjects were 26.27 (3.82) kg/m2 and 1.5 ± 1.5%, respectively. The median DII (range: –3.66 (most anti-inflammatory) to 4.31 (most pro-inflammatory)) was 0.75. Significant direct relationships were observed between the BMI and FAI (p < 0.001), HOMA-IR (p = 0.008), QUICKI (p = 0.002), testosterone (p < 0.001), FI (p = 0.017), FBS (p = 0.004), and Ferriman Gallwey score (p < 0.001). No significant associations were found between DII and the aforementioned biomarkers (p > 0.05). A normal BMI was associated with a significantly lower hirsutism score (β = –3.94, p = 0.003), fasting blood sugar (β = –10.02, p < 0.001), fasting insulin (β = –4.05, p = 0.042), HOMA-β (β = –1.20, p = 0.012), QUICKI (β = –0.19, p = 0.015), testosterone (β = –0.34, p < 0.001), and free androgen index (β = –0.96, p = 0.025) compared to an obese BMI after adjusting for confounders. No significant associations were observed for DII categories (median split) across any biomarkers or hirsutism.
Adiposity (measured by BMI)—not dietary inflammation—was independently associated with key PCOS manifestations, demonstrating significant positive relationships with hyperandrogenism markers (FAI, testosterone), insulin resistance (HOMA-IR), and clinical hirsutism. A normal BMI was correlated with clinically meaningful reductions in metabolic-androgen parameters compared to obesity. Thus, weight loss and a generally healthy diet may need to be combined to impact PCOS features significantly.
Calcium plays a central role in gastrointestinal (GI) physiology through regulating smooth muscle contractility, acid secretion, epithelial barrier integrity, and immune signaling. The dysregulation of calcium homeostasis has been increasingly implicated in the pathogenesis of GI disorders, including colorectal cancer, inflammatory bowel disease, peptic ulcer, and pancreatitis. Specifically, aberrant calcium-sensing receptor (CaSR) signaling has emerged as a critical molecular mechanism in colorectal tumorigenesis; meanwhile, calcium-mediated pathways influence gastric acid production and intestinal motility. This review critically evaluated recent advances in calcium signaling within the GI tract, highlighting the crosstalk involved with the gut microbiota and the roles of downstream effectors, including transient receptor potential vanilloid type 6 and store-operated calcium entry. This review also examined the therapeutic implications of calcium supplementation across various GI conditions, including bioavailability challenges under different disease states and nutrient interactions involving vitamin D and phosphate. Our review further addresses the role of calcium in mucosal immunity, the clinical relevance of hypocalcemia in GI diseases, and the potential of microbiome-guided nutritional interventions. However, despite growing mechanistic insights, considerable gaps remain in understanding host–microbiota–calcium interactions, genotype-specific responses to calcium, and long-term clinical outcomes. Thus, future research should clarify the dose–response relationships, stratify patient populations by CaSR polymorphisms and microbiome profiles, and establish precision strategies for calcium-based interventions in digestive health.
Selenium, a trace element with antioxidant properties, plays a vital role in the metabolism of microorganisms. Meanwhile, supplementation with selenium may also modify the activity of probiotics. Thus, this study aimed to analyze the effect of selenium supplementation on the growth, tolerance, and selenium binding capacity of two probiotic strains: Lactiplantibacillus plantarum DSM24730 and 299v. In particular, this study aimed to determine whether introducing this microelement into the culture environment would affect the growth capacity and detoxification mechanisms of these bacteria. Additionally, the ability of the selected strains to absorb and store selenium was analyzed, which could have potential benefits for both human health and the quality of probiotic preparations.
Bacterial cultures of Lactiplantibacillus plantarum DSM24730 and 299v were grown in specially prepared media supplemented with different concentrations of selenium (0–100 mg/L). This study assessed several key physiological parameters of microorganisms in real-time, including biomass production, growth dynamics, and the ability to survive in conditions that simulate the gastric and intestinal environments.
Growth curves and biomass analyses revealed that moderate selenium concentrations (5–10 mg/L) supported the growth of both strains, whereas higher concentrations (50–100 mg/L) inhibited biomass production and delayed the onset of growth, especially in DSM24730. Intensive growth of bacterial biomass (0.23 g/L; p < 0.05) in the experimental medium supplemented with 5 mg Se4+/L was observed for L. plantarum 299v after 24 h of cultivation. In the case of the DSM24730 strain, the lag phase (Δtlag) was prolonged at higher selenium concentrations, reaching 12 h at 100 mg/L, while the logarithmic phase (Δtlog) was shortened from 12 h in the control medium to only 2 h at 100 mg/L. The 299v strain demonstrated faster growth, higher biomass yield, and more rapid selenium uptake at moderate concentrations, while DSM24730 accumulated higher final levels of selenium after prolonged incubation. The highest selenium content (0.45 mg Se4+/g; p < 0.05) after 72 hours of cultivation was accumulated by strain L. plantarum 299v. Meanwhile, after the same culture time, the second bacterial strain (DSM24730) accumulated only 0.29 mg Se4+/g; p < 0.05). Tolerance assays using simulated gastric and intestinal fluids demonstrated that both strains survived under acidic gastric conditions; however, the viability of these strains significantly declined in intestinal juice at selenium concentrations of ≥10 mg/L, indicating an apparent dose-dependent inhibitory effect.
These observations suggest that 299v is more efficient in rapid selenium assimilation and biomass formation, while DSM24730 may be more suitable for high-capacity selenium loading over time. These findings are consistent with other studies on selenium-enriched probiotics, highlighting strain-specific responses to selenium supplementation. Strain selection and selenium dose optimization are essential for developing safe and effective selenium-enriched probiotic products.