Objectives: 

Both 17beta-estradiol and testosterone are known to induce insulin resistance in supraphysiological doses reached in some pharmacological usage such as anabolic drugs in sport's doping, some pathology such as PCOS or in physiological states as the pregnancy. But little is known about this negative role of the sex hormones on glucose metabolism. The aim of this study is to understand some of the molecular mechanisms underlying that process.

Materials: 

For this propose, human skeletal muscle cell cultures were acutely treated (4 hours) with either testosterone or 17beta-estradiol (10mM). The employment of specific inhibitors of some kinases was used to determine the specific pathways involved in this process. After the treatment, glucose incorporation into glycogen and the phosphorylation rates of some key protein were measured both in basal and insulin stimulated conditions.

Results: 

Both testosterone and estradiol treatments resulted in a significant decrease in glucose incorporation into glycogen. The pharmacological specific inhibition of the conventional PKCs almost restored the glycogen synthesis to baseline levels, in its combination with both, testosterone and 17beta-estradiol.

Conclusions: 

Our preliminary findings may suggest a negative role of acute exposure to high concentrations of sex hormones, on glucose incorporation into glycogen, that seems to be mediated by an over activation of the conventional PKCs, may indicate a metabolic shift from glucose toward palmitate metabolism.