Must be acylated at Ser3 (by GOAT enzyme) for GHSR-1a binding. Receptor activation in the pituitary stimulates GH release; hypothalamic action via NPY/AgRP neurons increases appetite and reduces energy expenditure.

N-terminal truncation eliminates IGFBP binding, leaving nearly all circulating IGF-DES unbound and active. Results in substantially higher tissue IGF-1R activation versus native IGF-1 at equivalent doses. Activates PI3K/Akt/mTOR for muscle hypertrophy and satellite cell proliferation.