title: Diabetes mellitus induces vaginal tissue fibrosis by TGF-beta 1 expression in the rat model.
abstract: The commonly reported sexual problem in women with diabetes mellitus is lack of vaginal lubrication. It is our hypothesis that reduced vaginal lubrication in diabetic women may result from the structural changes of the vagina. The aim of this study was to investigate in the diabetic rat model the vaginal structures using histochemistry and the expression of TGF-beta 1 using immunohistochemistry. Twenty female Sprague-Dawley rats (200-210 g) were divided into two groups: control and experimental. The experimental group (n = 10) received intravenous injection of streptozotocin (50 mg/kg). After 4 weeks, blood glucose levels were measured, and the vagina of the rat was excised. Serial sections of the vagina were used to perform hematoxylin and eosin (H & E) and Masson's trichrome stains, and for immunohistochemistry to identify TGF-beta 1 expression. The mean blood glucose concentrations were 67 +/- 11 mg/dL (range; 50-85) in the control group and 522 +/- 61 mg/dl (range; 429-590) in the experimental group. In the diabetic animals, vaginal tissue revealed reduced epithelial layers and decreased vaginal submucosal vasculatures compared to the control animals. The collagen connective tissue in the submucosal area of the diabetic animal tissue showed a dense and irregular, distorted arrangement. The immunoreactivity of TGF-beta 1 in the diabetic animals was prominent in the collagen connective tissue, fibroblasts, and smooth muscle fibers, whereas no immunoactivity was detected in the vaginal structures of the control animals. Diabetes mellitus may induce vaginal tissue fibrosis by TGF-beta 1 expression in the rat model. This implies that reduced vaginal lubrication in the diabetic women may result from the structural changes of the vagina.
authors.affiliation: Department of Urology, Chonnam National University Medical School, 5, Hakdong, Dongku, Kwangju 501-190, Korea. kpark@chonnam.ac.kr
authors.forename: K
authors.initials: K
authors.lastname: Park
authors.forename: S B
authors.initials: SB
authors.lastname: Ryu
authors.forename: Y I
authors.initials: YI
authors.lastname: Park
authors.forename: K
authors.initials: K
authors.lastname: Ahn
authors.forename: S N
authors.initials: SN
authors.lastname: Lee
authors.forename: J H
authors.initials: JH
authors.lastname: Nam
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000009:adverse effects; D001786:Blood Glucose / Q000378:metabolism; D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000139:chemically induced; D005260:Female; D005355:Fibrosis / Q000150:complications / Q000378:metabolism / Q000473:pathology; D007150:Immunohistochemistry; D009130:Muscle, Smooth / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013311:Streptozocin / Q000009:adverse effects; D016212:Transforming Growth Factor beta / Q000378:metabolism*; D053773:Transforming Growth Factor beta1; D014621:Vagina / Q000378:metabolism* / Q000473:pathology*
chemical_list: D000900:Anti-Bacterial Agents; D001786:Blood Glucose; C508962:Tgfb1 protein, rat; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D013311:Streptozocin