الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Obesity is a major public health issue worldwide and is frequently associated with erectile dysfunction (ED). Both conditions may share an internal pathologic environment, also known as common soil. Their main pathophysiologic processes are oxidative stress, inflammation, and resultant insulin and leptin resistance.
Moreover, the severity of ED is correlated with comorbid medical conditions, including obesity. Therefore, amelioration of these comorbidities may increase the efficacy of ED treatment with phosphodiesterase 5 inhibitors, the first-line medication for patients with ED.
Leptin, a key hormone in energy homeostasis and neuroendocrine function, has a permissive role in the pathogenesis of reproductive dysfunction in several states of energy imbalance. Leptin is the protein product of the Ob gene produced primarily by white adipose tissue such that its blood level correlates with body fat stores as a regulator of food intake and energy expenditure.
Testosterone deficiency is associated with a decline in erectile function and testosterone levels are inversely correlated with increasing severity of erectile dysfunction. Erectile dysfunction can be caused by multifactorial pathologies.
PDE 5 inhibitors are also used to treat erectile dysfunction. This is because the body has the same type of cells in the blood vessels of the lungs as the blood vessels of the penis.
The most commonly used PDE5 inhibitor drugs are sildenafil, vardenafil, tadalafil, and avanafil. These medications themselves do not produce erections in men, but allow them to achieve an erection and maintain this erection when there is sexual stimulation.
The study is aimed to assess the serum leptin and free and total testosterone in obese and none-obese men with erectile dysfunction and the response to phosphodiesterase type 5 inhibitors (PDE type 5 inhibitors) in obese and non-obese men with erectile dysfunction