Abstract
Erectile dysfunction (ED) is a long-term complication of type 2 diabetes (T2D) widely known to affect the quality of life. Several aspects of altered metabolism in individuals with T2D may help to compromise the penile vasculature structure and functions, thus exacerbating the imbalance between smooth muscle contractility and relaxation. Among these, advanced glycation end-products and reactive oxygen species derived from a hyperglycaemic state are known to accelerate endothelial dysfunction by lowering nitric oxide bioavailability, the essential stimulus of relaxation. Although several studies have explained the pathogenetic mechanisms involved in the generation of erectile failure, few studies to date have described the efficacy of glucose-lowering medications in the restoration of normal sexual activity. Herein, we will present current knowledge about the main starters of the pathophysiology of diabetic ED and explore the role of different anti-diabetes therapies in the potential remission of ED, highlighting specific pathways whose activation or inhibition could be fundamental for sexual care in a diabetes setting.
Highlights
Erectile dysfunction (ED) is a common underestimated complication of diabetes mellitus that affects more than 50% of people with diabetes [1,2]
Several experimental and clinical data have highlighted the ability of glucoselowering drugs to improve endothelial dysfunction and preserve endothelial cell viability
Since endothelial dysfunction represents a key event in the development of atherosclerosis, as well as of ED, the potential role of these agents in ED and the related molecular mechanisms are under investigation
Summary
Erectile dysfunction (ED) is a common underestimated complication of diabetes mellitus that affects more than 50% of people with diabetes [1,2]. Obesity and visceral fat accumulation, typically observed in subjects with T2D, collectively represent one of the main risk factors for secondary hypogonadism [5]. The association of visceral obesity with the hyperglycaemic/dyslipidaemic milieu and the combination of low circulating testosterone levels and the development endothelial dysfunction, macrovascular and microvascular disease, and diabetic neuropathy can significantly alter the fine mechanisms involved in regular erectile function. Substantial differences in the mechanism of action, glucose-lowering efficacy and effects on body weight and other cardiovascular risk factors of each drug may explain a potential variable impact on erectile function. This review sought to report on the selective effects demonstrated by glucose-lowering medications on erectile function and explore the potential mechanisms involved
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