Glaxon Cheat and Why To Buy It

This Joey Savage from Glaxon and on this Supplement Lab we're gonna get to talk about Glaxon Cheat. This gonna involve the insulin signalling pathway and PK, and a couple other fun things we're gonna talk about. These pathways are really really complex. I am by all intents and purposes omitting the details that are not going to be pertinent to the ingredients that are in here and what we're actually going to discuss on this. So this is more complex but I'm simplifying the heck out of it. I'm going to tell you about a whole bunch of different three and four letter acronyms.

So getting right into it this is the insulin signalling pathway insulin. On its own is a peptide hormone. It's responsible for glucose uptake and the downstream effects that occur past the insulin receptor. Now the insulin receptor is actually made out of two different types of subunits the alpha-subunits that are mounted in the plasma membrane, and then the beta-subunits 
which is located just below that.

When insulin comes into contact with this it causes a 3D conformational change, and this beautiful phenomenon occurs at the beta parts of the receptor called autophosphorylation, which means that they don't necessarily need to be catalysed by anything in order to phosphorylate themselves and transmit that signal further down the pathway. If you think about this it's like dominoes that you've lined up and you're going to knock them all down right well. Usually insulin is usually that first domino that gets knocked over and onto the rest of them. However if you skip that part you can actually knock down the rest of the dominoes while omitting the first couple of steps, which we'll get into.

So after the 3D conformational changes in the alpha subunits, the autophosphorylation and the beta-subunits, you have this third thing called the IRS. There's four different IRSs which are called the insulin receptor substrates. Now they regulate a few different things in activation of the insulin receptor. Substrates can knock all the rest of those dominoes as well. This is usually a protein that's going to be inhibited by something called PTP1B, which is a protein tyrosine phosphatase.

By blocking that you also allow the rest of the dominoes to flow. So going from the insulin receptor substrate it activates something called phosphatidylinositol 3 kinase and activates PIP3 and PDK, which is pyruvate dehydrogenase. These 2 things locked in a protein kinase C, But after that it'll activate AKT, which PKC and AKT will also activate AS160, which is the trigger event that actually gets the GLUT4 glucose transporter proteins to go ahead and go up and embed into the plasma membrane.

After AKT and after this whole glucose transport thing, it has effects on glycogen storage. It would inhibit glycogen synthase kinase 3B, which is something that usually normally represses glycogen synthase. So if you inhibit something that inhibits something else, you allow glycogensynthase. For example, to make more glycogen.

Now there's this other thing called glycogen phosphorylase. It's responsible for the conversion of glycogen back into glucose. A process also known as gluconeogenesis. It's also a natural process that occurs whenever your body actually needs to generate more glucose as fuel when you have plentiful amounts of stored glycogen.

The second pathway we're going to talk about is AMPK. Now AMPK stands for adenosinemonophosphate or AMP activated kinase. So usually when cellular energy levels are low ATP levels are gonna be low, and adenosine monophosphate levels are actually gonna be high, and this triggers AMPK. Now AMPK is also involved in a lot of energy sensing type mechanisms, especially in the sense of ATP, but it also has a lot of downstream effects.

Now AMPK is something that will inhibit mTOR so if you're actually looking to increase protein synthesis and get some pretty good muscle gains, AMPK activation might not actually be something that's viable on your menu. However if you're looking to increase more glucose and increase glycogen storage which is an energy kind of thing, then AMPK is a really good way to go in that sense. AMPK also inhibits cholesterol synthesis and also inhibits fatty acid synthesis and it also activates glycolysis, which is the natural process of breaking down sugars to form ATP in the first place.

Another thing that AMPK will do is it will block another regulatory protein called TBC1D1. This is something that is another inhibitor that usually blocks the activity of AS160 and like we just talked about before, when you block something that usually blocks something, you get a net positive. So by blocking this through AMPK it releases the chains of being held still to AS160, and as we said earlier AS160 is the actual trigger event which will bring glucosetransporters to the plasma membrane so you can absorb glucose.

The third different pathway we're going to talk about will actually be, basically the simple breakdown of carbohydrates and sugars, and this we usually occur at the intestinal brush border. There are different enzymes called alpha-glucosidase, alpha amylase, maltase and iso-maltase. There's a lot of different enzymes it will break down more complex carbohydrates into actual sugar molecules themselves.

The last pathway we're going to talk about, are the PPARs pathways so there's three, or kind of four different PPARs. They stand for peroxisome proliferator-activated receptor. These are usually different types of receptor proteins that are bound to your actual DNA and they control the expression of different genes involved in adipocyte differentiation activation of beta-oxidation and uncoupling.

So you can even override the whole beta-oxidation thing, but PPAR-gamma is going to be referred to, as that's the one that is for fat cell differentiation. You want to make more fat cells activate PPAR-gamma. The second one is PPAR-alpha which has huge range of different effects, however for all intents and purposes we'll talk about it in the sense of fatty or fat oxidation genes or the genes that are necessary for beta-oxidation. The last one, which is probably my favourite is PPAR-delta, which is also involved in beta-oxidation, but it's also involved in uncoupling proteins which are the override of actual glycolysis or beta-oxidation. You have the spontaneous generation of heat. This is also something that's going to be activated by exercise a lot of PPAR-delta agonists are also referred to exercise magnetics because of this.

Now that I've bored you with four different pathways we're gonna go ingredient by ingredient. Stuff you're familiar with to stuff you're not so familiar with, and it will always be in the context of insulin signaling pathway, AMPKA pathway, is it playing with the sugar metabolism at the intestinal brush border? or is it a PPAR activator deactivator kind of thing.


So chromium everybody knows chromium. Chromium is probably in just about every GDA that exists and in Glaxon Cheat we have chromium dinicocysteinate, which according to the literature has been proven to be the most efficacious form of chromium, and they pretty much attribute that to the actual extra cysteine that's there with the Zychrome.

Chromium is something that will activate AMPK theoretically, and all the other research that was done previously there was a lot of thought that went into why is chromium something that increases glucose sensitivity. It actually increases the translocation of GLUT4 to the plasma membrane but it doesn't embed.

Now AMPK can actually cause the embedding of GLUT4 into the plasma membrane but it's really something that's going to be dictated by insulin. So chromium in that sense will have a synergistic activity with insulin if you have normal insulin levels. So not only does it do that, it helps the GLUT4 translocation but it also works on a protein called LKB1. This is something that is sensitive to the AMP to ATP ratio, but is also an activator of AMPK, as well. So the net effect of taking chromium is it decreases membrane cholesterol, and by decreasing membrane cholesterol you actually have a more fluid plasma membrane where the glucose transporters can more readily embed into the cell membrane itself. That's basically the mechanism of chromium. It works off the AMPK pathway to increase GLUT4 for translocation of the plasma membrane.


The second thing that you'll see in a lot of GDA products is cinnamonn. Now to differentiate there's more than one kind of cinnamon. There's regular Chinese sentiments cinnamomum cassia and then there's the Ceylon cinnamon, the original true cinnamon that's native to Sri Lanka.

Cinnamon is something that has been shown to increase expression of the insulin receptor. It's also been shown to increase the expression of the insulin receptor substrate. In addition to that it increases hepatic glycogen, but it usually does this by increasing glycogen synthase expression. It also will be something that will inhibit GSK3B. So by inhibiting the inhibitor and by also increasing the expression of the glycogen synthase, you get higher glycogen amounts. Now it also will activate AMPK.

There's a lot of different active ingredients in cinnamon and it's a controversial topic as far as what actual active ingredient in cinnamon bark actually does the work. It's not a real clear answer because it appears to be more than one active component doing it, but cinnamaldehyde, the main component that's in cinnamon bark is something that will activate AMPK and cause GLUT4 translocation once again to the plasma membrane so glucose can be brought in.


Third thing is berberine. A lot of people like berberine and it is super hot right now. Not only because it's an AMPK activator but because it has effects that are comparable to metformin. There have been studies for a lot of these ingredients that showed comparability to metformin, but specifically berberine is the one gotten the most fame and hype.

Now it will increase the actual genetic expression of two different subtypes of AMPK. Both the alpha form which is in the cytosol and in the beta form which is inside of the nucleus. It will also increase glucose location like many of the other ingredients through the same kind of pathway but it also increases a smaller subtype of glucose transporter called GLUT1. It also increases insulin receptor expression, it increases IRS2 expression and it's also a PPAR-alpha and delta, not an agonist but something that also increases the expression of those two genes. As I had said earlier those are from beta oxidation uncoupling and more of the finer genes that control that

It's also an inhibitor of PPAR-gamma which is the fat cell differentiation gene, so it shuts off the ability to do that to varying degrees.


Next is maslinic acid. which is something that increases insulin receptor beta-substrate or insulin receptor beta-autophosphorylation, which is that second domino inline knocking down the rest, and by virtue of that it will increase GLUT4 ranslocation. It also will activate AKT through that same mechanism. By doing that it will also inhibit GSK3B and it will also inhibit the two different enzymes in the stomach alpha-amylase and glucosidase that are responsible for breaking down higher-order carbohydrates into their single subunits.


Corosolic acid which is the next one on this list is something that inhibits PTP1B and as I said earlier PTP won't be is something that inhibits the autophosphorylation events at the insulin receptor beta. By blocking a blocker once again we have a net positive effect which allows the auto phosphorylation of insulin receptor beta to occur.

There's also the ability for corosolic acid (because of this autophosphorylation event) to activate the downstream. Obviously once again we have glucose transporters being delivered to the plasma membrane, and it also works on LKB1 just like the cytochrome we talked about earlier. If this is something that's going to activate AMPK we have a completely separate mechanism where GLUT4 once again is translocated to the plasma membrane.

It also inhibits alpha-glucosidase (like i just said about maslinic acid) at the intestinal brush border. It is also an inhibitor of PPAR-gamma like berberine is, so it stops fat cell differentiation to a varying degree.


The last ingredient were going to talk about is bitter melon which probably my favourite. Bitter melon will inhibit PTP1B be allowing autophosphorylation and insulin receptor beta-subtype. It also increases IRS1 phosphorylation. Then because of that once again we're knocking down the rest of the dominoes down the line.

We also have GLUT4 translocation as a downstream effect, but something that's unique about bitter melon is it works off of adiponectin which is what is called an adipokine, a signalling molecule that comes from fat cells. Adiponectin is something that will cause a downstream cascade where it activates AMPK once again. This is going to be inhibiting cholesterol synthesis, triglyceride synthesis and so on and so forth. In addition to that we also have the activation of PPAR-alpha and gamma.

Now the weird thing about bitter melon when you're activating PPAR-alpha and you're increasing beta oxidation, and also by activating PPAR-gamma, you have more fat being burned. You have an increase in cell number. The clinical outcome of this is you have an increase in total number of fat cells, but they're smaller, much much smaller, so it's it's a weird kind of trade-off with bitter melon. In addition to that the downstream genes that are affected by PPAR-gamma activation from bitter melon like fatty acid synthase and acetylcholine carboxylase. Those downstream genes are actually downregulated, so even through some weird kind of finagling of the PPAR-gamma gene we can end up getting activation, which ends up making more cells but it compromises the ability for them to actually make fat. So that was kind of weird but it's cool.

The last thing about bitter melon is it's a PPAR-delta activator. Now the PPAR-delta is probably the most special of all the different PPARs that exist. Bitter melon had an effect on PPAR-delta and an increased its expression about 1.5 times over normal levels. In addition to that it also increased the promoter region protein that actually helps the transcription PPAR-delta 1.5 times as well. So once again PPAR-delta is something that's going to increase fat oxidation but it's also something that's going to increase uncoupling protein, which is something that's going to end up increasing the overall energy level and thermogenic effect.


Now on taking Glaxon Cheat, which is a six capsule a day dose we recommend that if you're goning to do three meals a day do two capsules one hour prior to consuming food. We say this because it's in a Dr-Cap, so it takes about 60 minutes in order to get to the small intestine, so we want to take these things at least an hour before consuming food. If you're not eating three meals a day and you're probably doing two and some snacks you'll want to take three capsules before your largest two meals of the day. Other than that you know this is gonna cause a noticeable ecrease in blood sugar, so you will probably get a little hypoglycemic. You don't want to take Glaxon Cheat and not eat because you're probably going to end up wanting to take a long nap.  It just will naturally make you tired because your energy levels get so low, but this could shift you into more of a fat-burning state. At the same time if you do consume carbohydrates Glaxon Cheat is more conducive to making you store more glycogen and burn more fat then not doing anything at all.

If you want better glucose absorption we'redoing it in like six different ways the other two things that are in this product of pine-bark anthocyanins which are really good for blood flow and pomegranate which if you know anything about gallotannins and ellagic acid and what happens when it comes into contact with your microbial colonies that live inside your small intestine... That'll be a little bread crumb for either we'll probably talk about in a later article, but do a little digging on this you might find something cool anyway. Anyway, that's been Glaxon Cheat, enjoy it!

Written by Joey Savage. Edited by Dino Tassigiannis. Originally published on YouTube at

  • Jun 17, 2020
  • Category: Blog
  • Comments: 0
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