Just for the record, injecting IGF-1 into the abs is not synonymous with injecting IGF-1 sub-q.
We need to distinguish this difference as abs are abdominals and that would be IM. Sub-q hs nothing to do with abs, Other than the fact that is the most common sub-q location (between the abdominals and skin). Sub-q can be done under the skin in many places in the body...
That being said, another note on dosage and delivery type (sub-q/IM).
If you are primarily looking for muscle cell agonism by IGF, IM makes more sense. Why? Well, because if you weigh 200lbs and want to maximally agonise your bicep (or abs or whatever muscle group) and inject 50mcg of IGF-1 sub-q, you have just injected 50mcg per 200lbs of body weight (0.25 mcg/lb). Without getting into complex science, I will guestimate that each lb of muscle will get an amount of IGF-1 closer to .025mcg/lb than the same 50mcg dose IM.
With IM the local muscle group receptor saturation will be exposed to the maximum amount of the same IGF dose before the rest goes sytemic. I'm sure it is quite obvious you have given the particular muscle group a greater exposure to the same dose of IGF-1 this way even if the remainder of IGF-1 ends up systemic.
Now, I have no real world proof of what systemic doses/duration one can be exposed to before gut growth is a concern.
I do know many claim to have decent fat loss with IGF-1 use. The mechanisms by which IGF-1 reduces lipogenesis in adipose tissue is not fully understood, however this study does draw some conclusions that IGF does not directly agonise adiposites as they do not have functional Type I IGF-1 receptors. The belief is that the actual mechanism lies in the decrease of insulin levels in the body from exogenous IGF-1. Given this it seems unlikely that sub-q IGF-1 for local fat burning is necessary as IM would affect this proposed method of action just the same as sub-q. This is however just another drawn conclusion from "another" study...
Who knows, we may possibly find out the method of action may be the weaker binding of IGF-1 to the IR (insulin receptor) in adipose tissue, occupying the receptor and keeping it from binding with insulin...
Anyhow, sorry for the rambling.. Just throwing out related interesting stuff (at least to me)
http://ajpendo.physiology.org/cgi/content/full/278/4/E729
IGF-I is believed to mediate some of the effects of GH via endocrine and paracrine mechanisms (14, 17, 40). However, direct effects of IGF-I in the liver and adipose tissue are unlikely, because these tissues lack functional type I IGF receptors (18, 29). IGF-I inhibits both GH (17, 18, 29) and insulin secretion (18, 27, 29, 36), further indicating an intimate relation between these hormones in the regulation of growth and metabolism.
Our results suggest that IGF-I reduces body fat mass via an inhibition of the lipogenic capacity of adipocytes. IGF-I probably reduces lipogenesis in adipose tissue via inhibition of insulin secretion. Moreover, an increased catecholamine-inducible lipolysis may also contribute to reduced body fat mass. In view of the present results and previous reports, it seems appropriate to conclude that IGF-I plays an important role in the regulation of intermediary metabolism, serving as a modulator of the effects of GH and insulin in this regulation. The potential of IGF-I for treatment of type II diabetes is further substantiated in this study by the findings of a decreased lipogenesis in adipose tissue and an insulin-like effect in skeletal muscle.