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The Effects of Short-Chain Fatty Acids in Urological Diseases
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Hee Jo Yang, Doo Sang Kim
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Urogenit Tract Infect 2022;17(1):8-13. Published online April 30, 2022
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DOI: https://doi.org/10.14777/uti.2022.17.1.8
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Abstract
PDFPubReaderePub
- The gut microbiome, believed to serve as a second genome within the human body, is involved in the regulation of several metabolic processes. These include human gene expression, development, nutrition and homeostasis. Dysbiosis, is an imbalance in the gut microbiome, which is known to be associated with various disease conditions such as Crohn's disease and Clostridium infections. The gut microbiota communicates with the host through a variety of biomolecules, nutrient signal-independent pathways, and epigenetic mechanisms. The gut microbiota supports the digestion and absorption of food, metabolizes fiber into bioactive short-chain fatty acids (SCFA), produces vitamins and nutrients, maintains gut integrity, and modulates host immunity. Among the above, there has been great interest in SCFA in microbiome research due to its beneficial effects on the intestinal barrier function and systemic anti-inflammatory effects. Recent reports have also indicated the role of SCFA in obesity, insulin resistance, and type 2 diabetes. While SCFA are associated with reduced risk of various diseases, dysbiosis and altered SCFA fermentative pathways could result in disease. This article is a review on the role of SCFA in urological diseases.
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Potential Mechanisms Underlying the Increased Excitability of the Bladder Afferent Pathways in Interstitial Cystitis/Bladder Pain Syndrome
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Doo Sang Kim
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Urogenit Tract Infect 2018;13(2):26-34. Published online August 31, 2018
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Abstract
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- Interstitial cystitis/bladder pain syndrome (IC/BPS) is a chronic debilitating disorder associated with lower urinary tract symptoms, including frequency, urgency, and suprapubic pain, which inconveniences the patients and seriously impairs their quality of life. Although the etiology of IC/BPS is unknown, intense research has been conducted focusing on the involvement of the bladder afferent nerve in regard to the cellular mechanisms underlying neurogenic inflammation of the urinary bladder. The involvement of neurogenic inflammation in patients with IC/BPS is supported by several animal models of bladder inflammation as well as clinical studies. Chronic bladder inflammation can result in functional and anatomical changes in the primary afferent neurons through the expression of inflammation-related proteins/receptors in the urinary bladder and bladder afferent pathways, leading to pain symptoms in patients with IC/BPS. In addition, neurogenic inflammation of the bladder mucosa can induce the central sensitization as well as the peripheral sensitization, and the neuroimmune overactivity and toll-like receptor (TLR) signaling of the immune cells involve complex mechanisms of central sensitization. This review presents the potential mechanisms underlying the afferent hyperexcitability of the bladder in IC/BPS and summarizes the neurogenic inflammation, neurotrophic factors, TLRs, and neuroimmune communication.
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