HyperSteroids - Effects of steroid hormone-related muscle hypertrophy and atrophy on systemic glucose homeostasis and adiposity

Hypertrophy and atrophy of skeletal muscle and adipose tissue are controlled by opposing actions of sexually dimorphic steroid hormones like androgens and glucocorticoids. In men, androgens promote muscle hypertrophy, insulin sensitivity, and reduce adiposity. In contrast, androgens in women promote insulin resistance, and increase visceral adiposity and type 2 diabetes risk. High physiological or pharmacological levels of glucocorticoids
promote muscle atrophy, impair insulin sensitivity, and increase adiposity. However, molecular mechanisms mediating these effects are not yet fully elucidated. Both androgens and glucocorticoids play various genomic and non-genomic roles regulating skeletal muscle glucose uptake, but our understanding of this biology is incomplete. In this project we will close these knowledge gaps by using advanced methods of metabolic research to investigate metabolic flux, inter-organ metabolism and metabolic health effects of steroid-induced muscle hypertrophy and atrophy in female and male mice as well as primary human myotubes from women and men.