Gut Microbiota Disorders in Obesity-Associated Benign Prostatic Hyperplasia in Rats.

Benign prostatic hyperplasia (BPH), commonly seen in older men, can cause symptoms of discomfort, and may even need surgical intervention. Studies have shown the potential link between gut microbes and BPH, but the molecular association is not fully understood. METHODS: Four-week-old male Sprague-Dawley rats (n = 16) were randomly allocated to normal control diet (ND, 10% fat) and high-fat diet-induced BPH (HFD, 45% fat) groups. Metagenomic analysis was used to examine the abundance and discrepancies in gut microbiota within the two groups after 24 weeks of feeding. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis was conducted to assess the biological functions of the differentially expressed genes. RESULTS: Rats with HFD-induced obesity exhibited morphological abnormalities in their prostate tissues. Metagenomic analysis of the gut revealed that Firmicutes were the dominant phyla in the HFD group, whereas the ND group had a higher abundance of Spirochaetes. At the genus level, Ruminococcus spp exhibited greater abundance in the HFD group, whereas Treponema spp were more abundant in the ND group. KEGG analysis demonstrated that the differentially expressed genes were mainly enriched in the NOD-like receptor (NLR) signaling, PI3K-Akt signaling, estrogen-signaling, signalings associated with GABAergic synapses, pantothenate and CoA biosynthesis. CONCLUSION: The findings of our study indicated that there was a notable variation in the microbiota abundance within the intestinal tract of obese rats suffering from prostate hyperplasia. It is plausible that these differentially abundant bacteria played a role in the development of pathological alterations in the prostate through the facilitation of inflammatory responses; however, additional research is required to validate the findings.

Gut microbiota in the association between obesity and kidney function decline: a metagenomics-based study in a rat model.

OBJECTIVES: Obesity can induce dysbiosis in the gut microbiota and is considered a separate risk factor for kidney function decline. Nonetheless, the precise function of intestinal microorganisms in facilitating the connection between obesity and kidney function decline remains uncertain. Hence, the objective of this study was to investigate the alterations in the gut microbiota composition that take place during obesity and their correlations with renal function utilizing a rat model. METHODS: For 20 weeks, 25 Sprague-Dawley rats were fed either a high-fat diet (HFD) or a normal-fat normal diet (ND). Physiological indices, peripheral plasma, kidney tissue, and colon contents were collected for comparison between groups. Metagenomic analysis of intestinal flora was performed. RESULTS: The HFD group demonstrated significantly increased levels of creatinine and urea nitrogen in the peripheral blood. Additionally, the HFD rats exhibited a significantly larger glomerular diameter compared to the ND group, accompanied by the presence of glomerulosclerosis, tubular vacuolar transformation, and other pathological changes in certain glomeruli. Metagenomics analysis revealed a notable rise in the prevalence of the Firmicutes phylum within the HFD group, primarily comprising the Rumenococcus genus. Functional analysis indicated that the gut microbiota in the HFD group primarily correlated with infectious diseases, signal transduction, and signaling molecules and interactions. CONCLUSIONS: This study provides evidence that the consumption of a HFD induces modifications in the composition and functionality of the gut microbiome in rats, which may serve as a potential mechanism underlying the relationship between obesity and the progression of kidney function decline.

Genetic association between membranous nephropathy and malignancies: a two-sample Mendelian randomisation study.

BACKGROUND: Various studies have reported that individuals with membranous nephropathy (MN) exhibit an elevated susceptibility to cancers. However, a causal relationship has not been clearly established. METHODS: We constructed a genetic score that predicts MN by utilizing genetic variants linked to this condition as instrumental variables. These genetic scores were then compared with lung, colon, breast, and prostate cancer risks by a two-sample Mendelian randomisation analysis involving the following methods: MR-Egger, weighted median, inverse variance weighted, simple mode, and weighted mode. RESULTS: This study demonstrated a lack of empirical substantiation for a causal association between genetic variants in MN and the susceptibility to lung, colon, prostate, or breast cancer. CONCLUSION: Overall, we did not detect a causal link between MN and lung, colon, breast, or prostate cancer. Hence, additional research is imperative to elucidate the underlying factors contributing to the heightened occurrence of tumour in patients with MN.