Effect of Androstenedione on Adipogenesis in Murine C3H10T1/2 Mesenchymal Cells
Effect of Androstenedione on Adipogenesis in Murine C3H10T1/2 Mesenchymal Cells作者机构：Department of Biochemistry Kirksville College of Osteopathic Medicine A.T. Still University of Health Sciences Kirksville MO USA Division of Endocrinology Charles R. Drew University of Medicine and Science Los Angeles CA USA Department of Health and Life Sciences Charles R. Drew University of Medicine and Science Los Angeles CA USA
出 版 物：《Open Journal of Endocrine and Metabolic Diseases》 (内分泌与新陈代谢疾病期刊（英文）)
年 卷 期：2015年第5卷第2期
页 面：9-18页
学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
主 题：Androstenedione Adipogenesis Myogenesis Androgen Receptor Bicalutamide
摘 要：Clinical trials of weak androgen androstenedione (AD) administered at a high concentration, showed an increase in muscle mass in men like strong androgens testosterone (T) and dihydrotestosterone (DHT), but did not show any inhibitory effect on fat mass unlike strong androgens. This observation prompted us to check the in-vitro effect of AD on adipogenesis using mouse mesenchymal multipotent cells (C3H10T1/2), which can differentiate into both myoblasts and adipocytes. Results indicated that AD inhibited adipogenesis at 10 nM, 100 nM and 1 μM concentrations, but not at 10 μM concentration. AD did not inhibit adipogenesis at 10 μM concentration and also did not inhibitmyogenesis at 10 μM concentration. Addition of bicalutamide, an androgen receptor (AR) antagonist decreased myogenesis and increased adipogenesis, indicating that the effect of AD was mediated through AR. Another weak androgen dehydroepiandrosterone (DHEA) also showed the same pattern of adipogenesis in 10T1/2 cells. AD also showed a similar pattern of adipogenesis in 3T3-L1 preadipocyte cells. Thus, the in-vitro results of AD on adipogenesis correlated with the in-vivo results of AD on fat-mass from clinical trials and suggested a possible difference in biological action between weak androgens (AD, DHEA) and strong androgens (T, DHT) on adipogenesis. Since the biological action of AD was mediated through AR, this physiological difference onadipogenesis could be due to the nature (partial agonist/antagonist) of AD binding to AR.
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