Ecdysteroids work in insects by binding to a receptor called the ecdysone nuclear receptor (EcR); however, no similar receptor has been found in mammals. In humans, the actions of ecdysteroids must therefore be through a different mechanism.[1] Given the broad range of effects that ecdysteroids may have in mammals, more than one mechanism of action is possible.
Ecdysteroids may act through a G-protein coupled receptor (GPCR), a receptor found on cell membranes that plays a role in cellular signaling. Specifically, ecdysteroids might bind to GPCRs found in the renin-angiotensin system (RAS) — an important regulator of fluids, blood volume, and vasodilation that acts within the kidney. Ecdysteroids activate the MAS1 proto-oncogene (genes that regulate cell growth and differentiation) within this system, and this could enhance muscle protein synthesis.[2][3]
Ecdysterone also causes an influx of calcium ions into the cells, which causes an increase in the phosphorylation of Akt. Akt is a protein kinase that mediates protein synthesis, so if ecdysterone increases its activity, then this could be the mechanism through which it enhances muscle growth.[4]
Finally, a type of estrogen receptor called estrogen receptor beta (ERβ) might be responsible for the actions of ecdysteroids in humans. The activation of ERβ has been related to muscle protein synthesis, and ecdysteroids have been shown to activate this receptor.[2]
The current data on how ecdysteroids work in mammals, and particularly in humans, is limited, and further research into the mechanisms of action is needed.