Mulletsoldier
Binging on Pure ****ing Rage
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If you remember, I wrote a small article on AP’s mechanism of action for both Striated Muscle and Adipocytes. In that article, I said the following regarding PPAR Gamma 2:
I’ve come across some recent research done on rats (I know, I know) that could suggest some more promise for Anabolic Pump. In this article, it was cited:
We hypothesize that AP, by modulating PPAR Gamma 2, is denying adipocytes both the ability to accumulate blood-lipids, and glucose. This is fairly significant, as by modulating PPAR Gamma 2 itself, AP is inducing a fasting effect specific for adipocytes. As the research shows, fasting itself is lowering both PPAR Gamma 2 levels and mRNA expression in adipose tissues. What this means in layman’s terms is that dosing Anabolic Pump is denying the fat cell's ability to take in fuel; conversely, this should induce a fasting effect that should further lower levels of PPAR Gamma 2 in adipocytes, leading to extended fat loss.
Further, the article cited the following:
This is a beneficial statement for Anabolic Pump as well, as AP exponentially increases the translocation of GLUT4 to the plasma membrane of Striated Muscle cells. Being far more permeable to glucose than natural, less Insulin should be required in order to maintain proper cell function. As the above statement suggested, those mice with Insulin-Deficient Diabetes were suppressing the expression of PPAR Gamma 1 & 2 by 75%. How this becomes significant for us, is this research suggests that lower levels of circulating Insulin may downregulate PPAR Gamma 2.
Basically, Anabolic Pump is creating an environment which works synergistically with the product. By denying a fuel source for adipocytes, it may have a fasting effect which lowers levels of PPAR Gamma 2. By increasing plasma membrane permeability, it may also lead to lower levels of circulating Insulin, which in turn will once again lower levels of PPAR Gamma 2. These both lead to a deficient ability of fat cells to bind to blood lipids, and glucose, which should cease their hypertrophy.
Please keep in mind this study was done on Rat adipocytes, as with many studies, so the results cannot be conclusive. I just found this to be extremely interesting and would be a good point to share. These are only my thoughts, and not facts.
Regulation of PPAR gamma gene expression by nutrition and obesity in rodents.
Vidal-Puig A, Jimenez-Linan M, Lowell BB, Hamann A, Hu E, Spiegelman B, Flier JS, Moller DE.
Department of Medicine, Beth Israel Hospital, Boston, Massachusetts 02215, USA.
I’ve come across some recent research done on rats (I know, I know) that could suggest some more promise for Anabolic Pump. In this article, it was cited:
We hypothesize that AP, by modulating PPAR Gamma 2, is denying adipocytes both the ability to accumulate blood-lipids, and glucose. This is fairly significant, as by modulating PPAR Gamma 2 itself, AP is inducing a fasting effect specific for adipocytes. As the research shows, fasting itself is lowering both PPAR Gamma 2 levels and mRNA expression in adipose tissues. What this means in layman’s terms is that dosing Anabolic Pump is denying the fat cell's ability to take in fuel; conversely, this should induce a fasting effect that should further lower levels of PPAR Gamma 2 in adipocytes, leading to extended fat loss.
Further, the article cited the following:
This is a beneficial statement for Anabolic Pump as well, as AP exponentially increases the translocation of GLUT4 to the plasma membrane of Striated Muscle cells. Being far more permeable to glucose than natural, less Insulin should be required in order to maintain proper cell function. As the above statement suggested, those mice with Insulin-Deficient Diabetes were suppressing the expression of PPAR Gamma 1 & 2 by 75%. How this becomes significant for us, is this research suggests that lower levels of circulating Insulin may downregulate PPAR Gamma 2.
Basically, Anabolic Pump is creating an environment which works synergistically with the product. By denying a fuel source for adipocytes, it may have a fasting effect which lowers levels of PPAR Gamma 2. By increasing plasma membrane permeability, it may also lead to lower levels of circulating Insulin, which in turn will once again lower levels of PPAR Gamma 2. These both lead to a deficient ability of fat cells to bind to blood lipids, and glucose, which should cease their hypertrophy.
Please keep in mind this study was done on Rat adipocytes, as with many studies, so the results cannot be conclusive. I just found this to be extremely interesting and would be a good point to share. These are only my thoughts, and not facts.
Regulation of PPAR gamma gene expression by nutrition and obesity in rodents.
Vidal-Puig A, Jimenez-Linan M, Lowell BB, Hamann A, Hu E, Spiegelman B, Flier JS, Moller DE.
Department of Medicine, Beth Israel Hospital, Boston, Massachusetts 02215, USA.
