Abstract
BackgroundCholesterol is mainly synthesised in liver and the rate-limiting step is the reduction of 3-hydroxy-3methylglutaryl coenzyme A (HMG-CoA) to mevalonate, a reaction catalysed by HMG-CoA reductase (HMGCR). There is a comprehensive body of evidence documenting that anabolic-androgenic steroids are associated with deleterious alterations of lipid profile. In this study we investigated whether a single dose of testosterone enanthate affects the cholesterol biosynthesis and the expression of HMGCR.Methods39 healthy male volunteers were given 500 mg testosterone enanthate as single intramuscular dose of Testoviron®--Depot. The total cholesterol levels prior to and two days after testosterone administration were analysed. Protein expression of HMGCR in whole blood was investigated by Western blotting. In order to study whether testosterone regulates the mRNA expression of HMGCR, in vitro studies were performed in a human liver cell-line (HepG2).ResultsThe total cholesterol level was significantly increased 15% two days after the testosterone injection (p = 0.007). This is the first time a perturbation in the lipoprotein profile is observed after only a single dose of testosterone. Moreover, the HMGCR mRNA and protein expression was induced by testosterone in vitro and in vivo, respectively.ConclusionHere we provide a molecular explanation how anabolic androgenic steroids may impact on the cholesterol homeostasis, i.e. via an increase of the HMGCR expression. Increasing knowledge and understanding of AAS induced side-effects is important in order to find measures for treatment and care of these abusers.
Highlights
Cholesterol is mainly synthesised in liver and the rate-limiting step is the reduction of 3-hydroxy3methylglutaryl coenzyme A (HMG-CoA) to mevalonate, a reaction catalysed by HMG-CoA reductase (HMGCR)
In this study we investigated whether a single dose of testosterone enanthate affects the cholesterol profile and the expression of HMGCR in healthy volunteers
There was no significant difference in high density lipoprotein (HDL), LDLD or VDL between day 0 and day 2
Summary
Cholesterol is mainly synthesised in liver and the rate-limiting step is the reduction of 3-hydroxy3methylglutaryl coenzyme A (HMG-CoA) to mevalonate, a reaction catalysed by HMG-CoA reductase (HMGCR). There is a comprehensive body of evidence documenting that anabolic-androgenic steroids are associated with deleterious alterations of lipid profile. Anabolic androgenic steroids (AAS) including testosterone, other endogenous androgenic hormones and synthetic substances structurally related to these compounds are the most frequently detected doping agents in the society and sports. The abuse of these agents for cosmetic purposes among non-competitive recreational body-builders and non-athletes is a considerable health concern. There is a comprehensive body of evidence documenting that AAS induce various deleterious alterations of the lipoprotein profile. The long-term consequences of these alterations are still unknown but it is possible that the perturbation of the lipid profile may be associated with an increase in risk of coronary artery disease
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