Hindawi Publishing Corporation International Journal of Endocrinology Volume 2010, Article ID 945053, 4 pages doi:10.1155/2010/945053 Research Article Alterations in Lipids and Adipocyte Hormones in Female-to-Male Transsexuals Prakash Chandra, 1 Sukhdeep S. Basra, 2 Tai C. Chen, 3 and Vin Tangpricha 1 1 Division of Endocrinology, Metabolism and Lipids, Department of Medicine, Woodruff Memorial Research Building, Room 1301, 101 Woodruff Circle NE, Atlanta, GA 30322, USA 2 School of Public Health, University of Texas at Houston, Houston, TX 77030, USA 3 Section of Endocrinology, Diabetes and Nutrition, Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA Correspondence should be addressed to Vin Tangpricha, vin.tangpricha@emory.edu Received 12 January 2010; Revised 6 April 2010; Accepted 9 June 2010 Academic Editor: Mario Maggi Copyright © 2010 Prakash Chandra et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Testosterone therapy in men and women results in decreased high-density lipoprotein cholesterol (HDL) and increased low-density lipoprotein cholesterol (LDL). We sought to determine whether testosterone therapy has this same effect on lipid parameters and adipocyte hormones in female-to-male (FTM) transsexuals. Twelve FTM transsexuals provided a fasting lipid profile including serum total cholesterol, HDL, LDL, and triglycerides prior to and after 1 year of testosterone therapy (testosterone enanthate or cypionate 50–125 mg IM every two weeks). Subjects experienced a significant decrease in mean serum HDL (52 ± 11 to 40 ± 7 mg/dL) (P<.001). The mean LDL (P = .316), triglyceride (P = .910), and total cholesterol (P = .769) levels remained unchanged. In a subset of subjects, we measured serum leptin levels which were reduced by 25% but did not reach statistical significance (P = .181) while resistin levels remained unchanged. We conclude that testosterone therapy in FTM transsexuals can promote an increased atherogenic lipid profile by lowering HDL and possibly reduce serum leptin levels. However, long-term studies are needed to determine whether decreases in HDL result in adverse cardiovascular outcomes. 1. Introduction Transsexualism is a medical condition characterized by gender dysphoria which is managed with cross-sex hormones and surgery to align an individual’s physical appearance with their gender orientation [1, 2]. Female-to-male (FTM) trans- sexuals take testosterone to change into a more masculine phenotype. Current guidelines remain uncertain about long effects of testosterone therapy on cardiovascular outcomes due to lack of long-term studies and suggest risk factors including lipids to be managed individually [1]. A recent meta-analysis of ten studies of testosterone therapy in FTM transsexuals by Elamin et al. demonstrated increased serum triglycerides (TG) and reduced high-density lipoprotein (HDL) concentrations. However, the data remained unclear about testosterone’s effects on other lipid fractions and blood pressure [3]. Other studies not examined in the meta- analysis by Elamin et al. have demonstrated increased total cholesterol (TC) [4] and low-density lipoprotein (LDL) lev- els [4, 5] in FTM transsexuals receiving testosterone therapy. Similarly, 17 FTM transsexuals treated with intramuscular injections of long acting testosterone undecanonate for 36 months demonstrated a decrease in TC and LDL without effecting triglyceride and HDL levels [6]. Gooren et al. [7] suggested that an increased atherogenic lipid profile can be a result increased weight and visceral fat after testosterone therapy in FTM transsexuals [8]. This changed adiposity pattern can lead to differential adipocyte hormone secretion [9, 10]. However, studies evaluating the effect of testosterone therapy on adipocyte hormones in FTM transsexuals are minimal and available data remain incon- clusive. While Elbers et al. [11] reported supraphysiological doses of testosterone in FTM to reduce leptin levels; others have failed to confirm this finding [12]. Similarly, the effect of supraphysiologic doses of testosterone administration on resistin still remains to be understood though endogenous