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Background: Childhood with obesity is characterized by metabolic dysregulation and unique gut microbiota profiles. Nevertheless, the comprehensive understanding of gut microbiota and metabolic dysregulation of Childhood with obesity remains unclear. Objectives: This study aimed to investigate the causal relationship of gut microbiota and Childhood with obesity and identify the blood metabolites as potential mediators. Methods: The exposure genome-wide association studies (GWAS) data were sourced from the GWAS Catalog, while the outcome GWAS data were obtained from the Early Growth Genetics (EGG) Consortium. The study used 473 types of gut microbiota, 233 types of blood metabolites, and Childhood with obesity from GWAS. We then performed two-sample Mendelian randomization (TSMR) and bidirectional Mendelian randomization (BDMR) analyses to explore the causal relationships between gut microbiota, blood metabolites, and Childhood with obesity. Additionally, we conducted multivariable Mendelian randomization (MVMR) and two-step Mendelian randomization (2SMR) to identify potential mediating blood metabolites in this process. Results: MR analysis identified 13 types of gut microbiota and 12 types of blood metabolites that were causally associated with Childhood with obesity. Furthermore, there was no strong evidence that genetically predicted Childhood with obesity had an effect on these gut microbiota and blood metabolites. Further, 2SMR analysis revealed that the association between K10 sp001941205 and Childhood with obesity was mediated by the Total cholesterol to total lipids ratio in medium VLDL, accounting for 2.53% (95%CI; 2.14%-2.92%) of the association. Similarly, the relationship between SM23-33 and Childhood with obesity was mediated by the Ratio of 22:6 docosahexaenoic acid to total fatty acids, which accounted for 4.07% (95%CI; 2.70%-5.44%) of the association. Conclusions: The present study is the first to investigate the causal relationships among 473 gut microbiota phenotypes, 233 blood metabolites, and Childhood with obesity through Mendelian randomization analysis, identifying 13 gut microbiota types with potential causal links to Childhood with obesity and suggesting that 2 blood metabolites may mediate these associations, thereby providing valuable insights for future intervention strategies aimed at addressing Childhood with obesity. Keywords gut microbiota, blood metabolites, mendelian randomization, Childhood with obesity
Background: Childhood with obesity is characterized by metabolic dysregulation and unique gut microbiota profiles. Nevertheless, the comprehensive understanding of gut microbiota and metabolic dysregulation of Childhood with obesity remains unclear. Objectives: This study aimed to investigate the causal relationship of gut microbiota and Childhood with obesity and identify the blood metabolites as potential mediators. Methods: The exposure genome-wide association studies (GWAS) data were sourced from the GWAS Catalog, while the outcome GWAS data were obtained from the Early Growth Genetics (EGG) Consortium. The study used 473 types of gut microbiota, 233 types of blood metabolites, and Childhood with obesity from GWAS. We then performed two-sample Mendelian randomization (TSMR) and bidirectional Mendelian randomization (BDMR) analyses to explore the causal relationships between gut microbiota, blood metabolites, and Childhood with obesity. Additionally, we conducted multivariable Mendelian randomization (MVMR) and two-step Mendelian randomization (2SMR) to identify potential mediating blood metabolites in this process. Results: MR analysis identified 13 types of gut microbiota and 12 types of blood metabolites that were causally associated with Childhood with obesity. Furthermore, there was no strong evidence that genetically predicted Childhood with obesity had an effect on these gut microbiota and blood metabolites. Further, 2SMR analysis revealed that the association between K10 sp001941205 and Childhood with obesity was mediated by the Total cholesterol to total lipids ratio in medium VLDL, accounting for 2.53% (95%CI; 2.14%-2.92%) of the association. Similarly, the relationship between SM23-33 and Childhood with obesity was mediated by the Ratio of 22:6 docosahexaenoic acid to total fatty acids, which accounted for 4.07% (95%CI; 2.70%-5.44%) of the association. Conclusions: The present study is the first to investigate the causal relationships among 473 gut microbiota phenotypes, 233 blood metabolites, and Childhood with obesity through Mendelian randomization analysis, identifying 13 gut microbiota types with potential causal links to Childhood with obesity and suggesting that 2 blood metabolites may mediate these associations, thereby providing valuable insights for future intervention strategies aimed at addressing Childhood with obesity. Keywords gut microbiota, blood metabolites, mendelian randomization, Childhood with obesity
Medical modulation of sex hormone levels is a cornerstone of treatment for many conditions that impact well-being, including cancer, fertility/infertility, gender dysphoria, and chronic metabolic diseases such as diabetes and obesity. The microbial residents of the intestine, known as the microbiota, interact with sex hormones in the intestine, and there is correlative evidence that this interaction is bidirectional. Based on these published findings, we hypothesized that transgender individuals receiving exogenous testosterone as part of their gender-affirming medical treatment might undergo changes in their intestinal microbiome. To test this, we collected 26 stool samples from nine individuals before and up to 8 months after initiation of treatment with exogenous testosterone and subjected these samples to metagenomic analysis. While no species were significantly associated with the duration of testosterone therapy, pathways that generate glutamate increased in abundance, while those that consume glutamate decreased. Glutamate is a precursor of arginine, and testosterone is known to increase levels of arginine and its metabolites in the plasma. We hypothesize that testosterone increases the uptake of glutamate by enterocytes, thus decreasing access of the microbiota to this amino acid. While this pilot study establishes the impact of testosterone therapy on the intestinal microbiome, a more comprehensive study is necessary to establish the impact of testosterone-driven metagenomic shifts on the stool metatranscriptome, the stool metabolome, and the plasma metabolome. IMPORTANCE The human intestine is inhabited by a large community of microbes known as the microbiome. Members of the microbiome consume the diet along with their human host. Thus, the metabolomes of the host and microbe are intricately linked. Testosterone alters the plasma metabolome. In particular, plasma levels of arginine and its metabolites and testosterone are positively correlated. To investigate the impact of exogenous testosterone on the microbiome, we analyzed the stool metagenomes of transgender individuals before and after the initiation of testosterone treatment. In this pilot project, we found a modest impact on the microbiome community structure but an increase in the abundance of metabolic pathways that generate glutamate and spare glutamate consumption. We propose that the host uses glutamate to generate arginine, decreasing the amount available for the microbiome.
Background. There is a lack of studies focusing on the combined impact of metformin, empagliflozin, and levothyroxine on the gut microbiota in patients with type 2 diabetes mellitus (T2DM) and hypothyroidism. The purpose of the study was to examine how the combination of metformin and empagliflozin affects gut microbiota composition in patients with type 2 diabetes and hypothyroidism. Materials and methods. We enrolled 47 patients who have been receiving hormone replacement therapy with levothyroxine at a stable dose over the past 2 years and were newly diagnosed with T2DM. All participants were divided into two groups and received either metformin alone or metformin plus empagliflozin for 6 months. Metabolic and hormonal parameters were measured before and after treatment, and stool samples were analyzed using PCR sequencing. Results. The study found that in both groups, there was an improvement in carbohydrate metabolism, lipid profile, and liver transaminases after treatment. The group treated with metformin plus empagliflozin had a more significant reduction in glucose, glycated hemoglobin, and atherogenicity coefficient than the group treated with metformin alone. We also found that combination therapy resulted in lower levels of Firmicutes and an increase in the number of Actinobacteria, as well as a higher ratio of Bacteroides fragilis to Faecalibacterium prausnitzii. Conclusions. The study shows for the first time that the combination of metformin, empagliflozin, and levothyroxine can directly affect the gut microbiota composition in patients with T2DM and hypothyroidism. These changes may be necessary for treating this cohort of patients and require further investigation.
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