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Androgen-Regulated Cardiac Metabolism in Aging Men

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...

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Autores principales: Barrientos, Genaro, Llanos, Paola, Basualto-Alarcón, Carla, Estrada, Manuel
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7243157/
https://www.ncbi.nlm.nih.gov/pubmed/32499759
http://dx.doi.org/10.3389/fendo.2020.00316
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author Barrientos, Genaro
Llanos, Paola
Basualto-Alarcón, Carla
Estrada, Manuel
author_facet Barrientos, Genaro
Llanos, Paola
Basualto-Alarcón, Carla
Estrada, Manuel
author_sort Barrientos, Genaro
collection PubMed
description 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.
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spelling pubmed-72431572020-06-03 Androgen-Regulated Cardiac Metabolism in Aging Men Barrientos, Genaro Llanos, Paola Basualto-Alarcón, Carla Estrada, Manuel Front Endocrinol (Lausanne) Endocrinology 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. Frontiers Media S.A. 2020-05-15 /pmc/articles/PMC7243157/ /pubmed/32499759 http://dx.doi.org/10.3389/fendo.2020.00316 Text en Copyright © 2020 Barrientos, Llanos, Basualto-Alarcón and Estrada. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Endocrinology
Barrientos, Genaro
Llanos, Paola
Basualto-Alarcón, Carla
Estrada, Manuel
Androgen-Regulated Cardiac Metabolism in Aging Men
title Androgen-Regulated Cardiac Metabolism in Aging Men
title_full Androgen-Regulated Cardiac Metabolism in Aging Men
title_fullStr Androgen-Regulated Cardiac Metabolism in Aging Men
title_full_unstemmed Androgen-Regulated Cardiac Metabolism in Aging Men
title_short Androgen-Regulated Cardiac Metabolism in Aging Men
title_sort androgen-regulated cardiac metabolism in aging men
topic Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7243157/
https://www.ncbi.nlm.nih.gov/pubmed/32499759
http://dx.doi.org/10.3389/fendo.2020.00316
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