Lipid Profile Changes Induced by Chronic Administration of Anabolic Androgenic Steroids and Taurine in Rats

• Published in: Medicina (Kaunas, Lithuania) Vol. 55; no. 9; p. 540
• Main Authors: Rosca, A.E., Stancu, Camelia Sorina, Badiu, Corin, Popescu, Bogdan Ovidiu, Mirica, Radu, Căruntu, Constantin, Gologan, Serban, Voiculescu, Suzana Elena, Zagrean, Ana-Maria
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI 27.08.2019; MDPI AG
• Subjects: AAS; anabolic androgenic steroids; Animals; cholesterol; Cholesterol - blood; DECA; Fatty Acids, Nonesterified - blood; HDL-C; lipids; Lipids - blood; lipoprotein; Male; nandrolone decanoate; Nandrolone Decanoate - pharmacology; Rats; Rats, Wistar; taurine; Taurine - pharmacology; triglycerides; Triglycerides - blood; DECA; HDL-C; anabolic androgenic steroids; lipids; AAS; lipoprotein; cholesterol; taurine; triglycerides; nandrolone decanoate
• ISSN: 1648-9144; 1010-660X; 1648-9144; 1010-660X
• DOI: 10.3390/medicina55090540

Background and Objectives: Anabolic androgenic steroids (AAS), used as a therapy in various diseases and abused in sports, are atherogenic in supraphysiological administration, altering the plasma lipid profile. Taurine, a conditionally-essential amino acid often used in dietary supplements, was acknowledged to delay the onset and progression of atherogenesis, and to mitigate hyperlipidemia. The aim of the present study was to verify if taurine could prevent the alterations induced by concomitant chronic administration of high doses of AAS nandrolone decanoate (DECA) in rats. Materials and Methods: Thirty-two male Wistar rats, assigned to 4 equal groups, were treated for 12 weeks either with DECA (A group), taurine (T group), both DECA and taurine (AT group) or vehicle (C group). Plasma triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), hepatic triglycerides (TGh) and liver non-esterified fatty acids (NEFA) were then determined. Results: DECA elevated TG level in A group vs. control (p = 0.01), an increase prevented by taurine association in AT group (p = 0.04). DECA decreased HDL-C in A group vs. control (p = 0.02), while taurine tended to increase it in AT group. DECA decreased TGh (p = 0.02) in A group vs. control. Taurine decreased TGh in T (p = 0.004) and AT (p < 0.001) groups vs. control and tended to lower NEFA (p = 0.08) in AT group vs. A group. Neither DECA, nor taurine influenced TC and LDL-C levels. Conclusions: Taurine partially prevented the occurrence of DECA negative effects on lipid profile, suggesting a therapeutic potential in several conditions associated with chronic high levels of plasma androgens, such as endocrine disorders or AAS-abuse.