Abstract
Sae-Chul Kim From the Department of Urology, Chung-Ang University College of Medicine, Seoul, Korea Insulin resistance is a hallmark of metabolic syndrome, including type 2 diabetes mellitus and obesity which are characterized by endothelial dysfunction. The endothelial dysfunction leads to erectile dysfunction (ED). Thus, understanding of insulin resistance is mandatory for urologists to understand a pathophysiology of ED. There are two distinct features of insulin signal transduction pathway. One is phosphatidylinositol 3-kinase-dependent pathway which regulates glucose uptake in skeletal muscle and nitric oxide (NO) production and vasodilation in vascular endothelium. In cavernous smooth muscles, insulin also induces the endothelium-dependent relaxation, however it may emanate from the direct inhibition of L-type Ca channels by prostacyclin in addition to NO production. The other one is mitogen-activated protein (MAP)-kinase pathway which regulates growth and mitogenesis and controls secretion of endothelin-1 in vascular endothelium. Stimulation of sympathetic activity by insulin may also contribute to hemodynamic regulation. A shift in balance between vasoconstrictor and vasodilator actions of insulin may be an important factor in the vascular pathophysology of insulin resistance, leading to ED. Hyperglycemia, elevated free fatty acid levels, and proinflammatory states share mechanisms between insulin resistance and endothelial dysfunction. There is evidence to suggest that testosterone is an important regulator of insulin sensitivity in men and hypotestosteronemia may have a role in the pathogenesis of insulin-resistant states. (Korean J Urol 2006;47:917-927) 대한비뇨기과학회지 제 47권 제 9호 2006
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