Diabetes Attenuates Female Genital Sexual Arousal Response via Disruption of Estrogen Action.
10.4111/kju.2009.50.3.211
- Author:
Abdulmaged M TRAISH
1
;
Tulay CUSHMAN
;
Richard HOYT
;
Noel N KIM
Author Information
1. Department of Biochemistry and Urology, Boston University School of Medicine, Boston, MA 02118, USA. atraish@bu.edu
- Publication Type:Review
- Keywords:
Diabetes mellitus;
Estradiol;
Testosterone;
Vagina;
Clitoris
- MeSH:
Animals;
Arousal;
Atrophy;
Clitoris;
Diabetes Complications;
Diabetes Mellitus;
Dyspareunia;
Estradiol;
Estrogens;
Female;
Genitalia;
Hemodynamics;
Humans;
Hyperglycemia;
Lubrication;
Models, Animal;
Plasma;
Progesterone;
Receptors, Androgen;
Receptors, Steroid;
Testosterone;
Vagina
- From:Korean Journal of Urology
2009;50(3):211-223
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Diabetes profoundly and negatively impacts all domains of female sexual function, however, the underlying pathophysiological mechanisms remain unknown. To date, limited studies have been published on the effects of type 1 & type 2 diabetes on female genital sexual arousal and how this may impact overall sexual function. The aim of this review is to discuss the effects of diabetes on female sexual function and insights from laboratory studies on the underlying pathophysiology. MATERIALS AND METHODS: Using PubMed, we reviewed and evaluated the literature published between 1970 and 2009 and data from our laboratories and others investigating the effects of type 1 and type 2 diabetes on genital sexual arousal responses. RESULTS: Women with diabetes experience diminished genital arousal, reduced vaginal lubrication, vaginal atrophy, dyspareunia, and increased vaginal infections. Also, a number of studies using type 1 and type 2 diabetic animal models have reported reduced plasma estradiol levels and marked physiological, biochemical and histological changes in genital tissues. In animal studies, diabetes alters genital tissue structure and attenuates expression of the estrogen, progesterone and androgen receptors and alters vaginal and clitoral hemodynamics. Importantly, treatment of diabetic animals with estradiol in the face of persistent hyperglycemia can restore vaginal structure and sex steroid receptor expression. CONCLUSIONS: Type 1 & type 2 diabetic complications produce significant structural and functional disruptions in genital organs and attenuate genital hemodynamics. In the type 2 animal model, estradiol treatment ameliorates diabetic-induced pathophysiological alterations in genital tissues, such as the vagina. This suggests that estrogen supplementation may be beneficial in restoring diabetes-induced genital pathology.
