Insulin Like Growth Hormone and Selective Glucose Uptake
Skinny Fats May Find Transformation Possible
So this is probably old news to a lot of those already well versed in the properties of insulin like growth factor 1 (igf-1), but for me it was a real eye opener when it comes to solving the problem of being “skinny fat”.First of all, the problem. Meet the skinny fat. They are a unique case of metabolic consequence. Usually we have the super skinny who don’t put muscle on easily but don’t gain fat easily either. We have the more traditional fatty which can put on muscle quite easily but gains a ton of fat in the process. You mesomorphs are going to find little of interest in here, so go back to looking amazing and putting on muscle just by putting away your groceries, you bastards.
The skinny fat, in my estimation is really just a fatty that starved themselves thin and are in a place where they can remain there but any attempts to put muscle on usually leads to excess fat gain, and any attempt to burn the fat off also burns the muscle off. They are pretty much metabolic syndrome posterchildren.
The solution? Undo the damage done that has caused metabolic syndrome. Keep insulin quiet. We can do that by limiting our carb intake. We can also do this by intermittent fasting. Another great way to keep insulin quiet is to utilize drugs or herbs that help sensitize our bodies to the effect of insulin. By doing so we reduce the amount and the duration of insulin production, thus keeping it quieter than normal.
A lot of people wish to have a magic chemical that would sensitize our muscles to insulin but not fat cells. While I agree this would be nice I think they’re missing the bigger picture. The bigger picture is that our carb intake has gotten out of control, like a spastic 2 year old with crayons, running amok in our body and causing a major stress. Insulin is the babysitter running after the kid, but in the process does more damage stomping around. Anything we can do to restore peace and tranquility to our metabolic system will, in the long run, be useful for fat loss and lean muscle gain. Sure, some of that glucose might get dumped into fat cells after converting to triglycerides, but the net effect is a restoration of our natural balance.
There seem to be two exceptions to this rule now. One way to effectively shuttle nutrients to muscle while ignoring fat is through intense exercise. After exercise our muscles are ready to suck up sugar without the help of insulin. Our glut-4 receptors come to the cell surface. Glucose Transporters normally need insulin to cajole their mouths open. Exercise removes this obstacle. Hungry muscles suck up sugar.
Another really awesome way I just learned about is the use of IGF-1. IGF-1 is like insulin, is produced from Growth hormone signalling in the liver, and mimics some of insulin’s effects except for one big difference. IGF-1 will dump glucose into a muscle cell, BUT it will NOT dump glucose into a fat cell. In essence we have that magic bullet people are dying for already. So how do we go about getting more igf-1?
IGF-1 LR3 is a unique form of IGF-1 that is synthesized artificially in order to avoid being bound by special proteins in the body. It’s really not such a bad thing if it did bind to a protein but I’m not going to get into that story. Because of these modifications IGF-1 LR3 is a perfect candidate for being a GDA (glucose disposal agent). It’s the most ideal GDA too because of it’s uniquely specific action on skeletal muscle.
While I’m not going to recommend anyone use IGF-1 LR3 I would say that if I were using it I would inject subcutaneously about 20 micrograms a day and keep my carbohydrates on the lowish side. More carbs than I would if I weren’t using it, but don’t go hog wild. Use for four weeks and then take two weeks off. Not because of receptor down regulation, which has been the commonly believed reason, but because of antibodies our immune system create to “protect” ourselves from this foreign invader.
It won’t be an overnight transformation, but over the course of six months I would imagine someone could have eliminated metabolic syndrome and would be on their way to the kind of body composition transformation all skinny fats wish they could achieve.
Different effects of IGF-I on insulin-stimulated glucose uptake in adipose tissue and skeletal muscle
The effect of insulin-like growth factor I (IGF-I) on insulin-stimulated glucose uptake was studied in adipose and muscle tissues of hypophysectomized female rats. IGF-I was given as a subcutaneous infusion via osmotic minipumps for 6 or 20 days. All hypophysectomized rats received l-thyroxine and cortisol replacement therapy. IGF-I treatment increased body weight gain but had no effect on serum glucose or free fatty acid levels. Serum insulin and C-peptide concentrations decreased. Basal and insulin-stimulated glucose incorporation into lipids was reduced in adipose tissue segments and isolated adipocytes from the IGF-I-treated rats. In contrast, insulin treatment of hypophysectomized rats for 7 days increased basal and insulin-stimulated glucose incorporation into lipids in isolated adipocytes. Pretreatment of isolated adipocytes in vitro with IGF-I increased basal and insulin-stimulated glucose incorporation into lipids. These results indicate that the effect of IGF-I on lipogenesis in adipose tissue is not direct but via decreased serum insulin levels, which reduce the capacity of adipocytes to metabolize glucose. Isoproterenol-stimulated lipolysis, but not basal lipolysis, was enhanced in adipocytes from IGF-I-treated animals. In the soleus muscle, the glycogen content and insulin-stimulated glucose incorporation into glycogen were increased in IGF-I-treated rats. In summary, IGF-I has opposite effects on glucose uptake in adipose tissue and skeletal muscle, findings which at least partly explain previous reports of reduced body fat mass, increased body cell mass, and increased insulin responsiveness after IGF-I treatment.
