Researchers publishing in Aging have explained a relationship between inflammation, metabolic syndrome, and prostate enlargement.
Not so benign
Benign prostatic hyperplasia (BPH) is only called ‘benign’ to differentiate it from another well-known cause of prostate enlargement: prostate cancer. BPH is known to lead to bladder obstruction and lower urinary tract issues. It also coincides with other diseases, including neurological and cardiovascular disorders along with diabetes [1].
Similarly, previous research has established a link between BPH and metabolic syndrome [2], the well-known combinatin of obesity, insulin resistance, high blood pressure, and related problems. Inflammation seems to be a likely cause [3], although it can be from multiple sources, not all of which are age-related [4]. Specifically, IL-17, an interleukin secreted by lymphocytes, activates an inflammatory pathway that activates further interleukins [5].
This work was conducted to confirm and expand on those previous findings by directly examining associations between metabolic syndrome, short-chain fatty acids, and interleukin expression in prostate tissue.
Metabolic syndrome seems to make things slightly worse
This study recruited 103 participants with BPH, 42 of whom had metabolic syndrome. All of these participants were qualified for transurethral resection of the prostate, a surgical procedure that involves cutting away excess tissue.
These two populations did not significantly differ in age or many other physical metrics. In general, they differed in ways that define metabolic syndrome, such as blood pressure and cholesterol. Interestingly, there were no statistically significant differences between the groups in inflammatory biomarkers, and their concentrations of these biomarkers in serum were comparable to healthy groups in other studies.
Tissue samples were slightly different. Increased IL-6 expression was slightly but significantly more visible in the prostate stromal cells of patients with metabolic syndrome, and there was more IL-18 in their prostate glandular cells.
A limited but existing connection
Despite these lukewarm results, the researchers were able to observe a critical correlation: men with less of the “good cholesterol” HDL had more IL-6 in their prostate glandular and stromal cells, whether they had metabolic syndrome or not. In men who were diagnosed with metabolic syndrome, this only applied to the stromal cells.
For IL-18, similar results were found for both triglycerides and HDL. The ratio of triglycerides and HDL, along with the relationship between LDL and HDL, were also found to have associations with this inflammatory compound. These relationships were more pronounced in men with metabolic syndrome.
Short-chain fatty acids were also found to be involved. There were limited associations between IL-18 and the SCFAs isocaproic acid and acetic acid in certain tissues and patient groups.
In total, metabolic syndrome apparently has an association with prostate enlargement in specific ways. However, this association is surprisingly limited. Further work in other areas should be done to determine why BPH is so common in men of advanced age and what can be done to combat this root cause.
Literature
[1] Parsons, J. K. (2010). Benign prostatic hyperplasia and male lower urinary tract symptoms: epidemiology and risk factors. Current bladder dysfunction reports, 5, 212-218.
[2] Gacci, M., Sebastianelli, A., Salvi, M., De Nunzio, C., Vignozzi, L., Corona, G., … & Serni, S. (2017). Benign prostatic enlargement can be influenced by metabolic profile: results of a multicenter prospective study. BMC urology, 17, 1-6.
[3] Gacci, M., Vignozzi, L., Sebastianelli, A., Salvi, M., Giannessi, C., De Nunzio, C., … & Maggi, M. (2013). Metabolic syndrome and lower urinary tract symptoms: the role of inflammation. Prostate cancer and prostatic diseases, 16(1), 101-106.
[4] De Nunzio, C., Salonia, A., Gacci, M., & Ficarra, V. (2020). Inflammation is a target of medical treatment for lower urinary tract symptoms associated with benign prostatic hyperplasia. World journal of urology, 38(11), 2771-2779.
[5] Krušlin, B., Tomas, D., Džombeta, T., Milković-Periša, M., & Ulamec, M. (2017). Inflammation in prostatic hyperplasia and carcinoma—basic scientific approach. Frontiers in Oncology, 7, 77.
