
Originally Posted by
tjax03
One thing that I would like to throw into this discussion that I do not believe has been mentioned yet are the effects of an insulin independent mechanism for glucose uptake into skeletal muscle. This comes to mind after reading Hartman's posting of this Eli Lilly info piece. Basically, it suggests that certain populations may be at a higher risk of diabetes in response to GH therapy (the obese, strong family history, inactive, etc). Now some of you may know this, and some may not, but the primary transporter for the uptake of glucose into both adipose (fat) and skeletal muscle cells is called GLUT4. It is a cell membrane bound protein that is regulated by two primary factors. The first is insulin. When insulin levels increase in response to a meal, GLUT4 molecules, which have been synthesized and stored within the cell, are then transferred to the cell surface/membrane, where they function to transport glucose into the cells for conversion to energy etc. In the case of insulin resistance, as seen in response to GH therapy, insulin will have less of an effect on increasing the amount of GLUT4 at the cell surface, allowing it to remain within the cell where it is useless. This has the effect of increasing blood glucose, and in combination with other factors, may result in the development of diabetes. However, GLUT4 within skeletal muscle is also regulated solely by the contraction of the muscle itself. I'm unsure of the exact mechanism, but basically when we flex our muscles, the structure of the muscle cell deforms slightly, which results in increased cell surface GLUT4 expression. What does all this really mean to you all? Well, if you are lifting weights consistently, you will be getting decent GLUT4 expression on the cell surface due to the previously mentioned mechanism. This will help to reduce any increase in blood sugar levels caused by GH use. Furthermore, and perhaps more desirable, this mechanism will result in increased shuttling of glucose into the muscles where we want it, while simultaneously reducing shuttling into adipose tissue. This is because the GLUT4 transport into fat cells is solely dependent on insulin sensitivity unlike the muscle cells where we can rely on the cellular pathways triggered by muscle contraction to aid in glucose uptake. I hope you all find this helpful in aiding you understanding and interesting.