Oh, got it. I was misreading your post and replacing IGF-1 with GH in my head.

This section of the study/article seems to be a little more on target...
"IGF-1 binds to insulin receptors with very low affinity; therefore its binding to IGF-1 receptors and/or hybrid insulin/IGF-1 receptors has been postulated to be the mediator of enhanced insulin action (12). IGF-1 does not bind to hepatocytes or adipocytes, and therefore its primary insulin-sensitizing action is believed to be mediated through skeletal muscle. Administration of IGF-1 to normal humans results in glucose lowering that is approximately one-twelfth as potent as that induced by insulin (13), and in patients with extreme insulin resistance it improves insulin sensitivity and carbohydrate homeostasis (14)."

However, the next paragraph is complicates this statement because IGF-1 also suppresses GH secretion...
"One problem in interpreting almost all human studies of IGF-1 has been that, in addition to enhancing insulin action, it also suppresses GH secretion; therefore it has been difficult to determine the relative roles of the direct actions of IGF-1 and those that are mediated by suppression of GH."