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From:
http://www.T-Nation.com/..._of_fat&cr=
Here's an interesting fact that you might not know. The fat cell (not the muscle cell) is a major regulator of how easily you gain muscle. It's the fat cell that sends all of the molecular signals for glucose and nutrient uptake in both fat and lean tissue. This is especially important because it's the nutrient uptake that has the most impact (not androgens) on gaining muscle.
As most advanced bodybuilders know, the most anabolic hormone in the body is insulin, not testosterone. Unfortunately, insulin is anabolic in both muscle and fat. But by decreasing the effects of insulin on fat and increasing the effects of insulin on muscle, you can achieve what no one thought was possible and turn the common man into a bodybuilding genetic freak.
As always, there are genetic limitations to how much muscle an individual can gain â?? C3G can't turn short muscle bellies into long muscle bellies. But I think we all understand that. The real issue at hand isn't the genetic limits on overall muscle size. The sad fact is, most people will never attain but a fraction of the gains they could â?? both in terms of muscle gains and overall leanness â?? due to their dysfunctional nutrient uptake.
"I Want to Get Big... I Want to Get Shredded... No, I Want to Get Big..."
Dysfunctional nutrient uptake results in what amounts to a bodybuilding identity crisis, where you go back and forth between trying to get big and trying to get shredded â?? but never truly achieving either goal.
You get bigger, alright, but it's mostly fat. You tend to rationalize it until the day you see some guy in the gym with razor-sharp etched muscle who has your look â?? at least, the one you've decided you want now. You're sick about what you've done to yourself, and with renewed vigor you're off to shredded-land. Except, at the end of that jaunt, you haven't etched anything and you're now "skinny," which totally ticks you off and sends you back the other direction.
This is obviously an irrational approach to achieving a lean and muscular body. But what's not so obvious is the cause of this dysfunction. It's due to a condition that's tantamount to "inflammatory fat disease."
Inflammatory Fat Disease
Most diseases of modern living have been linked to inflammation. So it's no wonder that researchers have found that inflammatory signaling has also caused fat cells to become dysfunctional, resulting in high circulating glucose levels, out of control appetite, fat cells that love to get "fatter," and lazy muscle cells that prefer to leave most of the fuel for the fat cells to gobble up and store.
This is where C3G comes in. The consensus among researchers is that C3G acts primarily (through the Glut4-RBP4 system) to optimize molecular crosstalk between fat cells, which directly decreases adipocyte inflammatory signals. The overall effect causes the body to repartition nutrients so that what you eat literally turns to muscle instead of fat.
In other words, your body resists storing fat, releases and oxidizes fat-cell content (fatty acids), and preferentially pulls glucose and nutrients into muscle cells.
The Effects of C3G on Target Tissues
Indigo-3GTM Repartitions Nutrients into Muscle Instead of Fat
Fat Cells â?? C3G actually up-regulates gene expression for fat oxidation (fat burning) and down-regulates gene expression for fat storage. The oxidation of fatty acids increases further directly through the release of adiponectin. The overall effect is that fat cells begin to shrink in size. The reduced inflammation also decreases the size of fat cells and disgorges the excess water associated with the inflammatory process (less bloated and squishy feeling to the fat under the skin).
Muscle Cells â?? Insulin sensitivity of muscle cells increases, thereby enhancing insulin signaling and glucose uptake, along with enhancing glycogen synthesis, which drives glucose and nutrients preferentially into muscle.
Liver Cells â?? Liver cells decrease gluconeogenesis via downregulation of glucose-6-phosphatase, preventing the liver from increasing circulating glucose levels.
GI Tract â?? Taken prior to meals, C3G decreases amylase and glucosidase, effectively decreasing the speed and extent of carbohydrate digestion.
That's what I3G says anyhow.
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