Efeito da dieta hiperlipídica/hipoproteica e esteroide anabolizante sobre o perfil lipídico, níveis de citocinas, morfologia e função hepática em camundongos

Abstract

Dyslipidemias exhibit high prevalence worldwide and are strongly associated with the occurrence of cardiovascular diseases. Although the etiology of dyslipidemia is complex and multifactorial, the pathogenesis of these conditions has been associated to the food intake profile. In animal models, exposure to high-fat diets (HFD) constitutes robust experimental models to investigate the effect of dietary profile on metabolism, organ structure and function. Beyond interfere with cellular energy metabolism, use of supraphysiological doses of anabolic steroids has been often associated with high toxicity, causing renal, cardiovascular and liver diseases. It is well established that the food intake profile can increase or reduce the toxicity induced by several drugs, including hormones, offering a risk or protection factor to the organism. The present study investigated the effect of a HFD and anabolic steroid on body composition, lipid profile, liver function and structure in mice. Sixty C57BL/6 female, 12 weeks of age were randomized equally into 5 groups: Group 1: Standard Diet; Group 2: Standard Diet + testosterone cypionate (20 mg / kg); Group 3: HFD; Group 4: HFD + testosterone cypionate (10 mg / kg); Group 5: HFD + testosterone cypionate (20 mg / kg). When administered in animals fed a standard diet (normolipidic and normocaloric), the anabolic did not induce deleterious metabolic or morphofunctional changes in liver tissue. Conversely, anabolic was beneficial in reducing the circulating levels of LDL cholesterol and liver function enzymes in these animals. In combination with HFD, anabolic steroid worsened dyslipidemia, reducing circulating levels of HDL cholesterol, increasing triglycerides levels and the severity of hepatic steatosis in mice. Taken together, the results showed that HFD was able to interact with anabolic steroids in a complex way, modifying the characteristics of susceptibility and resistance to morphofunctional liver damage and systemic lipid metabolism dysfunction in mice.