High-density lipoprotein cholesterol is not decreased if an aromatizable androgen is administered.

TLDR: There were no changes in total cholesterol, triglycerides, or insulin in any group but, in the MeT group, apo AI levels decreased and low-density lipoprotein cholesterol (LDL-C) increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Abstract: We examined the influence of aromatization of testosterone on serum high-density lipoprotein cholesterol (HDL-C) and postheparin plasma hepatic triglyceride lipase activity (HTLA) in men. Eighteen healthy lean nonsmokers (ages, 20 to 33) were administered androgens in a weekly total dose of 280 mg for 12 weeks in one of three groups: testosterone enanthate (TE) (280 mg/wk intramuscularly [IM]); TE (280 mg/wk IM) + testolactone (TL) (250 mg orally [PO] four times daily); or methyltestosterone (MeT) (20 mg PO twice daily). Serum testosterone achieved steady state levels by 4 weeks with >40 nmol/L (TE and TE + TL) and 250 pmol/L (TE) or remained below 70 pmol/L (TE + TL and MeT). LH fell to less than 5 U/L (TE and TE + TL) but remained unchanged with MeT. By 4 weeks, HDL-C had decreased significantly from 1.20 ± 0.13 to 0.77 ± 0.13 mmol/L (MeT), from 1.18 ± 0.15 to 0.89 ± 0.13 mmol/L (TE + TL), and demonstrated no decrease in the TE group across the time course of the study. These changes were preceded by mean increases in HTLA of 102% (MeT) and 55% (TE + TL) over baseline, and no significant change with TE. The changes in HDL-C and HTLA returned to baseline within 2 weeks of steroid cessation. There were no changes in total cholesterol, triglycerides, or insulin in any group but, in the MeT group, apo AI levels decreased and low-density lipoprotein cholesterol (LDL-C) increased. After 12 weeks of treatment, sex hormone binding globulin (SHBG) levels were decreased to 37% (MeT), 54% (TE + TL), and 73% (TE) of baseline levels; these changes were evident by the second week of treatment and returned to baseline by the second week following treatment cessation. These results suggest that TE has little effect on HTLA but when a corresponding increase in E2 levels is prevented, HTLA increases. MeT, which is not metabolized to E2, produced the most dramatic HTLA increases, even at a dose that did not reduce serum LH; thus, hepatic specific properties of 17-alkylated androgens may further increase the atherogenic potential of this class of androgens.