Comparison of the gut microbiome composition between men with erectile dysfunction and a matched cohort: a pilot study.

BACKGROUND: To-date there have been minimal studies to investigate an association between the gut microbiome and erectile dysfunction. There have been many inflammatory diseases linked to gut microbiome dysbiosis; such as cardiovascular disease and metabolic syndrome. These same inflammatory diseases have been heavily linked to erectile dysfunction. Given the correlations between both conditions and cardiovascular disease and the metabolic syndrome, we believe that it is worthwhile to investigate a link between the two. OBJECTIVE: To investigate the potential association between the gut microbiome and erectile dysfunction. METHODS: Stool samples were collected from 28 participants with erectile dysfunction and 32 age-matched controls. Metatranscriptome sequencing was used to analyze the samples. RESULTS: No significant differences were found in the gut microbiome characteristics, including Kyoto Encyclopedia of Genes and Genomes richness (p = 0.117), Kyoto Encyclopedia of Genes and Genomes diversity (p = 0.323), species richness (p = 0.364), and species diversity (p = 0.300), between the erectile dysfunction and control groups. DISCUSSION: The association of gut microbiome dysbiosis and pro-inflammatory conditions has been well studied and further literature continues to add to this evidence. Our main limitation for this study was our small-sample size due to recruitment issues. We believe that a study with a larger population size may find an association between the gut microbiome and erectile dysfunction. CONCLUSIONS: The results of this study do not support a significant association between the gut microbiome and erectile dysfunction. Further research is needed to fully understand the relationship between these two conditions.

Comparative assessment of outcomes and adverse effects using two different intramuscular testosterone therapy regimens: 100 mg IM weekly or 200 mg IM biweekly.

This study aimed to compare the change in levels of several laboratory values and the development of adverse events using two commonly used intramuscular testosterone therapy regimens. Men were included if they were 18 years or older and received one of the following testosterone therapy regimens: 100 mg intramuscular once weekly or 200 mg intramuscular once every other week. Primary outcomes were relative changes in total testosterone, free testosterone, estradiol, prostate-specific antigen, and hematocrit at 6 months after initiation of testosterone therapy. Secondary outcomes were any significant rises in estradiol, hematocrit, prostate-specific antigen, and any other treatment-related adverse events requiring cessation of testosterone therapy. A total of 263 men were enrolled. In a subanalysis of men who had a baseline hematocrit below 54% before intramuscular testosterone therapy initiation, we found the following: men who received 100 mg weekly injections were significantly less likely to have hematocrit levels rising above 54% (1/102 (1%) vs. 4/51 (8%); p = 0.023). No significant differences were recorded in the increase in total testosterone, free testosterone, prostate-specific antigen, and estradiol levels between both groups. A higher average serum testosterone over the dosing interval seen with the 200 mg regimen appears to be associated with a higher risk of erythrocytosis.

Profiling of superoxide dismutase isoenzymes in compartments of the developing bovine antral follicles.

The antral follicle constitutes a complex and regulated ovarian microenvironment that influences oocyte quality. Oxidative stress is a cellular state that may play a role during folliculogenesis and oogenesis, although direct supporting evidence is currently lacking. We thus evaluated the expression of the three isoforms (SOD1, SOD2, and SOD3) of the enzymatic antioxidant superoxide dismutase in all the cellular (granulosa cells, cumulus cells, and oocytes) and extracellular (follicular fluid) compartments of the follicle. Comparisons were made in bovine ovaries across progressive stages of antral follicular development. Follicular fluid possessed increased amounts of SOD1, SOD2, and SOD3 in small antral follicles when compared with large antral follicles; concomitantly, total SOD activity was highest in follicular fluids from smaller diameter follicles. SOD1, SOD2, and SOD3 proteins were expressed in granulosa cells without any fluctuations in follicle sizes. All three SOD isoforms were present, but were distributed differently in oocytes from small, medium, or large antral follicles. Cumulus cells expressed high levels of SOD3, some SOD2, but no detectable SOD1. Our studies provide a temporal and spatial expression profile of the three SOD isoforms in the different compartments of the developing bovine antral follicles. These results lay the ground for future investigations into the potential regulation and roles of antioxidants during folliculogenesis and oogenesis.

Identification of androgen response elements in the insulin-like growth factor I upstream promoter.

Testosterone stimulates the expression of IGF-I in cells and tissues that include prostate, muscle and muscle satellite cells, and the uterus. Here, the molecular mechanisms of this effect of testosterone were explored. Testosterone increased IGF-I mRNA levels in HepG2 and LNCaP cells and stimulated the activity of reporter genes controlled by 1.6 kb of the upstream promoter of the human IGF-I gene. An androgen-responsive region that was located between -1320 and -1420 bases upstream of the first codon was identified by truncation studies. The androgen-responsive region was found to contain two sequences resembling known androgen receptor (AR)-binding sites from the Pem1 gene. Reporter genes incorporating these sequences were strongly stimulated by androgens. Each of the androgen-responsive elements (AREs) bound recombinant AR-DNA-binding domain in gel-shift experiments; binding was greatly enhanced by sequences flanking the apparent AR-binding half-sites. Testosterone induced recruitment of AR to sequences of genomic DNA containing these AREs. The two AREs were activated 5-fold more by AR than glucocorticoid receptor. Collectively, these findings indicate the presence of two AREs within the IGF-I upstream promoter that act in cis to activate IGF-I expression. These AREs seem likely to contribute to the up-regulation of the IGF-I gene in prostate tissues, HepG2 cells, and potentially other tissues.