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

Abstract

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.

Anabolic Steroids and Cardiovascular Outcomes: The Controversy

“…However, this study was limited to a short period of two months among a small group of 267 athletes. In 2019, three studies supported the claim that AS use was related to dyslipidemia [ 15 - 17 ]. Rosca et al conducted a study in rats and affirmed an increase in triglycerides and LDL with a decrease in HDL in plasma [ 15 ].…”

“…In 2019, three studies supported the claim that AS use was related to dyslipidemia [ 15 - 17 ]. Rosca et al conducted a study in rats and affirmed an increase in triglycerides and LDL with a decrease in HDL in plasma [ 15 ]. Souza et al highlighted the mechanism of AS use, and stated it impairs HDL leading to the decrease in efflux of cholesterol, and may lead to early coronary artery disease [ 16 ].…”

Capsaicin and Gut Microbiota in Health and Disease

“…We wonder what is the mechanism of TβMCA augmentation, especially as it appears to have the largest variation compared to all other tested conjugated-BA [94]. Probably, because taurine, a semi-essential amino acid, which has been shown to have numerous beneficial effects in the human body [105][106][107][108], also targets the intestine and it is known to regulate gut microbiota by inhibiting harmful bacteria, reducing bacterial lipopolysaccharide (LPS) level, and accelerating short-chain fatty acids (SCFA) production [109,110]. Moreover, homotaurine stimulates GABA receptors in capsaicin-sensitive sensory neurons [111]; taurine-derived bile salts interfere with gastric mucosal blood flow and secretion, by modulating these sensory neurons [112][113][114]; and CAP infusion in the extracellular fluid increases taurine concentration [115].…”

Oxandrolone Use Causes Dyslipidemia in Resistance-Training Practitioners

“…A study of HIV-infected men that was not controlled for antiretroviral intake treated with OX daily for 12 weeks and reduced HDL for all doses of OX studied [33]. In an animal model, OX elevated triglycerides, reduced HDL, decreased hepatic triglycerides, and elevated levels of non-esteri ed fatty acids produced by the liver, possibly leading to increased lipidic synthesis of hepatic triglycerides [113]. Additionally, OX may reduce blood triglycerides by further activation of the triglyceride lipase that results in hydrolysis of peripheral triglycerides.…”