Diabetes might adversely affect expression and function of interstitial cells in the urinary bladder and urethra in humans: a new mechanism in the development of diabetic lower urinary dysfunction?Med Hypotheses. 2011 May; 76(5):632-4.MH
Diabetes is an important disease affecting many people worldwide which causes significant morbidity. In the lower urinary tract (LUT), diabetes causes LUT dysfunction in humans by leading to neuropathic bladder. In addition, diabetes can lead to functional and anatomical abnormalities of the external urethral sphincter. Diabetes was suggested to cause these complications by affecting autonomic or peripheral nerves or both. Cells having similar characteristics with interstitial cells of Cajal that are present in the gastrointestinal system have also been described in the human urinary tract. Interstitial cells (ICs) in the urinary tract were suggested to function as pacemaker cells, stretch or chemical sensors that might trigger detrusor contractions which work with close relationship with the nerves. In the human urethra, ICs were suggested to control the frequency of tonic contractions of the urethral smooth muscle. Therefore, ICs seem be playing a very important role in LUT function in humans. The hypothesis in this paper suggests that diabetes might also adversely affect IC expression and IC function in the human LUT which might play a significant role in the development of diabetic LUT dysfunction. A search of the English literature was performed by using Medline/PubMed in order to search this hypothesis and no particular study was found in humans. The information and evidence obtained following the investigation of this hypothesis might uncover the possible underlying mechanism of decreased IC expression or function in addition to neuropathy in the development of diabetic LUT dysfunction. Currently, no specific medical drug treatment or preventive measure exists targeting the cellular components of the LUT (i.e. ICs and nerves) which are in fact responsible for a normally functioning LUT. If the expression and distribution of ICs are adversely affected in the LUT of patients with diabetes, specific drugs might be developed as targeted therapy stimulating IC function which could then be used to treat diabetic LUT dysfunction and benefit many diabetic patients worldwide. Moreover, having the knowledge of the IC expression and distribution status at the level of the LUT in patients with diabetes could be a possible prognostic factor for the clinicians indicating the risk of future LUT deterioration. Therefore, targeted therapy might also be used as to prevent the development of LUT dysfunction in this patient group.