ABSTRACT
Dehydroepiandrosterone (DHEA) is a precursor of sex steroid hormones and is converted to testosterone by 17β-hydroxysteroid dehydrogenase (HSD) and 3β-HSD enzymes (Labrie et al. 2005; Figure 4.1). We found that 3β-HSD, 17β-HSD, and aromatase cytochrome P450 (P450arom) existed in cultured skeletal muscle cells, and steroid hormones including testosterone were locally synthesized from DHEA in skeletal muscle (Aizawa et al. 2007); therefore, skeletal muscle is presumed to be capable of synthesizing and metabolizing sex steroid hormones. In a skeletal muscle specimen testosterone administration accelerated protein synthesis and anabolism (Urban et al. 1995), resulting in muscle growth and/or increased strength (Ihemelandu 1980). Thus, sex steroid hormones are important for muscle con‰guration and function. Sex steroid hormones generally decrease with aging, and it has been reported that a de‰ciency of sex steroid hormones in both men and women is a risk factor for developing obesity and type 2 diabetes (Ding et al. 2007). Yamaguchi et al. (1998) reported that patients with hyperinsulinemia had low DHEA levels. Therefore, lower sex steroid hormone levels may be related to the pathogenesis of obesity and type 2 diabetes.
