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Problem: Currently, there is a variety of evidence linking the gut microbiota to changes in sex hormones. In contrast, the causal relationship between SHBG, a carrier of sex hormones, and the gut microbiota is unclear. Method of Study: Bidirectional two‐sample Mendelian randomization (MR) analysis was used to detect the causal effect between SHBG and the gut microbiome. Summary statistics of genome‐wide association studies (GWASs) for the gut microbiome and SHBG were obtained from public datasets. Inverse‐variance weighting (IVW), weighted median, weighted mode, MR‐Egger and simple mode methods were used to operate the MR analysis. F‐statistics and sensitivity analyses performed to evaluate bias and reliability. Results: When we set gut microbiome as exposure and SHBG as outcome, we identified nine causal relationships. In males, Coprobacter (PIVW = 2.01 × 10−6), Ruminococcus2 (PIVW = 3.40 × 10−5), Barnesiella (PIVW = 2.79 × 10−2), Actinobacteria (PIVW = 3.25 × 10−2) and Eubacterium fissicatena groups (PIVW = 3.64 × 10−2) were associated with lower SHBG levels; Alphaproteobacteria (PIVW = 1.61 × 10−2) is associated with higher SHBG levels. In females, Lachnoclostridium (PIVW = 9.75 × 10−3) and Defluviitaleaceae UCG011 (PIVW = 3.67 × 10−2) were associated with higher SHBG levels; Victivallaceae (PIVW = 2.23 × 10−2) was associated with lower SHBG levels. According to the results of reverse MR analysis, three significant causal effect of SHBG was found on gut microbiota. In males, Dorea (PIVW = 4.17 × 10−2) and Clostridiales (PIVW = 4.36 × 10−2) were associated with higher SHBG levels. In females, Lachnoclostridium (PIVW = 7.44 × 10−4) was associated with higherr SHBG levels. No signifcant heterogeneity of instrumental variables or horizontal pleiotropy was found in bidirectional two‐sample MR analysis. Conclusions: This study may provide new insights into the causal relationship between the gut microbiome and sex hormone‐binding protein levels, as well as new treatment and prevention strategies for diseases such as abnormal changes in sex hormones. [ABSTRACT FROM AUTHOR]

Endometriosis (EM) in reproductive females has an incidence of 6–10% and greatly affects female fertility, quality of life, and long-term health. The gut microbiota can affect the physiological and pathological processes of humans through various pathways, such as those involving the nervous and endocrine systems and immunity, and it plays important roles in endocrine and inflammatory diseases. Whether the gut microbiota plays a role in EM has gradually attracted researchers' attention. In the present study, fecal and blood samples were collected from 12 patients with stage 3/4 EM and 12 healthy controls. We performed 16S rRNA high-throughput sequencing to compare the gut microbiota between the EM and control groups. Serum levels of hormones and inflammatory cytokines were measured. We found that compared with the control group, the EM group had a lower α diversity of gut microbiota and a higher Firmicutes/Bacteroidetes ratio. The abundances of various taxa (such as Actinobacteria, Tenericutes, Blautia, Bifidobacterium, Dorea, and Streptococcus) were significantly different between the two groups. The taxon with the highest abundance in the EM group was Prevotella_7, and that in the control group was Coprococcus_2. The serum levels of E2 and IL-8 were significantly higher in the EM group than in the control group (E2: EM group 74.7 ± 22.5 pg/L vs CON group 47.9 ± 12.5 pg/L; IL-8: EM group 6.39 ± 1.59 pg/mL vs CON group 4.14 ± 0.73 pg/mL). Additionally, the gut microbiota of the EM group was enriched for the microbial function categories environmental information processing, endocrine system, and immune system. Correlations were detected between each of Blautia and Dorea abundance and estradiol level and between Subdoligranulum abundance and IL-8 level. This study elucidated the associations between the gut microbiota and both serum hormones and inflammatory factors in EM. However, the findings need to be verified in future studies. [ABSTRACT FROM AUTHOR]

Problem: This study aims to investigate the effects of alpha‐linolenic acid (ALA) on the gut microbiota (GM) and the abdominal environment in mice with endometriosis (EMS). Methods: The effects of faecal microbiota transplantation (FMT) from EMS mice on mice treated with antibiotic cocktail were conducted. The 16S rRNA sequencing and PICRUSt software were used to detect the structure and function of GM respectively. The protein levels of Claudin 4 and ZO‐2 in the intestinal wall were detected using the western blotting. The level of LPS in the abdominal cavity was detected using enzyme‐linked immunosorbent assay (ELISA). The content of macrophages in the abdominal cavity was detected using flow cytometry. Results: The exogenous supplementation of ALA could restore the abundance of Firmicutes and Bacteroidota in EMS mice. After the ALA treatment, the abundance of 125 functional pathways and 50 abnormal enzymes related to GM in EMS mice was significantly improved (p <.05). The expression of the ZO‐2 protein in the intestinal wall was decreased, and the level of LPS in the abdominal cavity was significantly increased after FMT from EMS mice (p <.05). ALA could increase the expression of the ZO‐2 protein in the intestinal wall of EMS mice, reduce the level of LPS in the abdominal cavity (p <.05) and reduce the aggregation of peritoneal macrophages (p <.05). Conclusion: Alpha‐linolenic acid can improve the GM, intestinal wall barrier and abdominal inflammatory environment and reduce the level of LPS in mice with EMS. [ABSTRACT FROM AUTHOR]

Gut microbiota disorders are closely related to polycystic ovarian syndrome (PCOS). Buzhong Yiqi prescription (BZYQ) has a significant clinical effect on the treatment of patients with obesity exhibiting PCOS and phlegm-dampness syndrome caused by spleen deficiency (SPSD). Hence, this study aimed to explore gut microbiota and fecal metabolite alterations in such patients treated with BZYQ. Fifty eligible patients with obesity manifesting PCOS and SPSD participated and agreed to undergo 3 months of BZYQ treatment. Results showed that BZYQ significantly alleviated the serum dehydroepiandrosterone sulfate p < 0.001 and testosterone levels p < 0.001 and markedly changed the gut microbiota structure in these patients. Furthermore, 106 differential fecal metabolites and 14 KEGG enrichment pathways were quantified. The phylum Spirochaetae and the genera [Eubacterium]_rectale_group, Escherichia-Shigella, and Fusicatenibacter were significantly more abundant, but Megamonas was significantly less abundant after treatment than before treatment. Disorders in the gut microbiota and fecal metabolites of these patients were closely related to hyperandrogenemia and insulin resistance. In conclusion, BZYQ could ameliorate the serum androgen level and had an impact on the gut microbiota and metabolites in patients with obesity manifesting PCOS and SPSD. [ABSTRACT FROM AUTHOR]

Problem: Endometriosis (EMS) is a chronic inflammatory disease with unclear pathogenesis. Three studies have uncovered the influence of gut microbiota on mice with EMS, but no study has investigated the characteristics of fecal metabolomics to determine some important clues on EMS. This research aims to uncover the interaction between fecal metabolomics and gut microbiota in EMS mice. Method of study: Female C57BL/6J mice were used to construct the EMS model. Non‐target metabolomics was applied to detect the fecal metabolites of EMS mice. The 16s rRNA sequencing was used for clarifying the composition of the gut microbiota. The functional characteristics of gut microbiota were analyzed using the PICRUSt. The receiver operator characteristic curve (ROC) analysis was utilized for determining the potential important differential metabolites, and the Spearman correlation coefficient was applied for expressing the correlation between the important differential metabolites and gut microbiota. Results: A total of 156 named differential metabolites were screened. The diversity and the abundance of gut microbiota in EMS mice decreased. Eleven pathways were involved in the differential metabolites and the functional prediction of gut microbiota, among which the second bile acid biosynthesis and alpha‐linolenic acid (ALA) metabolism were the significant enrichment pathways. The increased abundance of chenodeoxycholic and ursodeoxycholic acids and the decreased abundance of ALA and 12,13‐EOTrE were found in the feces of EMS mice. Conclusion: The abnormal fecal metabolites, which are influenced by dysbacteriosis, may be the characteristics of EMS mice and can be the potential important indices to distinguish the disease. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to explore the relationship between the fecal metabolites and gut microbiota in obese patients with PCOS and provide a new strategy to elucidate the pathological mechanism of obesity and PCOS. Methods: The fecal samples of obese patients with PCOS (n = 18) and obese women without PCOS (n = 15) were analyzed by 16S rRNA gene sequencing and untargeted metabolomics. The peripheral venous blood of all subjects was collected to detect serum sex hormones. The association among fecal metabolites, gut microbiota, and serum sex hormones was analyzed with the R language. Results: A total of 122 named differential fecal metabolites and 18 enrichment KEGG pathways were obtained between the groups. Seven fecal metabolites can be used as characteristic metabolites, including DHEA sulfate. The richness and diversity of gut microbiota in the obese PCOS group were lower than those in the control group. Lachnoclostridium, Fusobacterium, Coprococcus_2 , and Tyzzerela 4 were the characteristic genera of the obese patients with PCOS. Serum T level significantly and positively correlated with the abundance of fecal DHEA sulfate (p < 0.05), and serum DHEAS level significantly and negatively correlated with the abundance of fecal teasterone (p < 0.05). Conclusion: Specific fecal metabolites may be used as characteristic metabolites for obese patients with PCOS. The closely relationship among gut microbiota, fecal metabolites, and serum sex hormones may play a role in the related changes caused by hyperandrogenemia. [ABSTRACT FROM AUTHOR]