Abstract
The prevalence of cardiovascular mortality is higher in men than in age-matched premenopausal women. Gender differences are linked to circulating sex-related steroid hormone levels and their cardio-specific actions, which are critical factors involved in the prevalence and features of age-associated cardiovascular disease. In women, estrogens have been described as cardioprotective agents, while in men, testosterone is the main sex steroid hormone. The effects of testosterone as a metabolic regulator and cardioprotective agent in aging men are poorly understood. With advancing age, testosterone levels gradually decrease in men, an effect associated with increasing fat mass, decrease in lean body mass, dyslipidemia, insulin resistance and adjustment in energy substrate metabolism. Aging is associated with a decline in metabolism, characterized by modifications in cardiac function, excitation-contraction coupling, and lower efficacy to generate energy. Testosterone deficiency -as found in elderly men- rapidly becomes an epidemic condition, associated with prominent cardiometabolic disorders. Therefore, it is highly probable that senior men showing low testosterone levels will display symptoms of androgen deficiency, presenting an unfavorable metabolic profile and increased cardiovascular risk. Moreover, recent reports establish that testosterone replacement improves cardiomyocyte bioenergetics, increases glucose metabolism and reduces insulin resistance in elderly men. Thus, testosterone-related metabolic signaling and gene expression may constitute relevant therapeutic target for preventing, or treating, age- and gender-related cardiometabolic diseases in men. Here, we will discuss the impact of current evidence showing how cardiac metabolism is regulated by androgen levels in aging men.
Highlights
The multifactorial origin of cardiovascular diseases compels a comprehensive approach that incorporates lifestyle modification with an appropriate selection of medications for energyregulation and its co-morbid conditions [1,2,3,4]
Many clinical publications over the past few years have indicated that very low levels of plasma testosterone are associated with pathophysiological processes, such as dyslipidemias, metabolic syndrome and diabetes type 2, which are considered as the underlying mechanisms involved in age-related cardiovascular diseases in men [19,20,21,22,23]
Recent reports indicate that testosterone therapy increases the expression of fibroblast growth factor 2 (FGF2) and decreases myogenic regulatory factor 4 (MRF4) and myostatin in skeletal muscle from men suffering hypogonadotropic hypogonadism, suggesting that the expression of these proteins contribute to muscle growth after testosterone therapy [65]
Summary
The multifactorial origin of cardiovascular diseases compels a comprehensive approach that incorporates lifestyle modification with an appropriate selection of medications for energyregulation and its co-morbid conditions [1,2,3,4]. Many clinical publications over the past few years have indicated that very low levels of plasma testosterone are associated with pathophysiological processes, such as dyslipidemias, metabolic syndrome and diabetes type 2, which are considered as the underlying mechanisms involved in age-related cardiovascular diseases in men [19,20,21,22,23]. As found in late-onset hypogonadism and elderly men, have been associated with different types of heart diseases [24, 25]. The relationship between metabolic and cardiovascular risk in humans is evident in men suffering from hypogonadism, a condition in which the reduced functional activity of the gonads causes a decrease in testosterone levels [42]. Recent reports indicate that testosterone therapy increases the expression of fibroblast growth factor 2 (FGF2) and decreases myogenic regulatory factor 4 (MRF4) and myostatin in skeletal muscle from men suffering hypogonadotropic hypogonadism, suggesting that the expression of these proteins contribute to muscle growth after testosterone therapy [65]
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