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Licensed Unlicensed Requires Authentication Published by De Gruyter October 1, 2011

Androgen deficiency and mitochondrial dysfunction: implications for fatigue, muscle dysfunction, insulin resistance, diabetes, and cardiovascular disease

Abdulmaged M. Traish EMAIL logo , Bassima Abdallah and George Yu

Abstract

Among the major physiological functions of steroid hormones is regulation of carbohydrate, fat, and protein metabolism. Mitochondria, through oxidative phosphorylation, play a critical role in modulating a host of complex cellular metabolic pathways to produce chemical energy to meet the metabolic demand for cellular function. Thus, androgens may regulate cellular metabolism and energy production by increased mitochondrial numbers, activation of respiratory chain components, and increased transcription of mitochondrial-encoded respiratory chain genes that code for enzymes responsible for oxidative phosphorylation. Androgen deficiency is associated with increased insulin resistance, type 2 diabetes (T2DM), metabolic syndrome, obesity, and increased overall mortality. One common link among all these pathologies is mitochondrial dysfunction. Contemporary evidence exists suggesting that testosterone deficiency (TD) contributes to mitochondrial dysfunction, including structural alterations and reduced expression and activities of metabolic enzymes. Here, we postulate that TD contributes to symptoms of fatigue, insulin resistance, T2DM, cardiovascular risk, and metabolic syndrome through a common mechanism involving impairment of mitochondrial function.


Corresponding author: Abdulmaged M. Traish, MBA, PhD, Professor of Biochemistry, Professor of Urology, Boston University School of Medicine, 715 Albany Street, A502, Boston, MA 02118, USA Phone: +1-617-638-4578, Fax: +1-617-638-5412

Received: 2011-10-11
Accepted: 2011-11-18
Published Online: 2011-10-01
Published in Print: 2011-10-01

©2011 by Walter de Gruyter Berlin Boston

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