Those people who have use GH therapy for years and taken morning fasted blood glucose tell me that GH usage pushed those numbers up. When they switched to GHRP-6/Mod GRF(1-29) those numbers came down.
They were happy because they were getting their therapy and had less diabetogenic effect.
One reason this may be so is that natural GH release is composed of a blend of isoforms. Two are equally anabolic: a 22kda form and a 20kda form
The 22kda form is the one used in synthetic GH and is 191 amino acids long.
The 20kda form is released naturally w/ 22kda. 20kda is identical however 15 amino acids in the part of the chain that interacts w/ the prolactin receptor are missing.
In rats 20kda produces less edema and less diabetogenic effect. In addition it doesn't interact w/ prolactin binding protein and has other characteristics a bit unique. In humans it is less clear if the side effects are less w/ 20kda then 22kda.
So using GHRH/GHRP to evoke a natural GH pulse means you get a blend of GHs (one of which is less diabetogenic).
That may be one reason.
All of the anecdotal feedback that I have received from diabetics tells me that the effect on blood sugar is less on the peptides then it is on synthetic GH.
Those people who have use GH therapy for years and taken morning fasted blood glucose tell me that GH usage pushed those numbers up. When they switched to GHRP-6/Mod GRF(1-29) those numbers came down.
They were happy because they were getting their therapy and had less diabetogenic effect.
The 20kda form is released naturally w/ 22kda. 20kda is identical however 15 amino acids in the part of the chain that interacts w/ the prolactin receptor are missing.
So using GHRH/GHRP to evoke a natural GH pulse means you get a blend of GHs (one of which is less diabetogenic).
IM TYPE 2 NO SPIKES WHAT SO EVER. AS THIS SUGGEST.
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Those people who have use GH therapy for years and taken morning fasted blood glucose tell me that GH usage pushed those numbers up. When they switched to GHRP-6/Mod GRF(1-29) those numbers came down.
They were happy because they were getting their therapy and had less diabetogenic effect.
One reason this may be so is that natural GH release is composed of a blend of isoforms. Two are equally anabolic: a 22kda form and a 20kda form
The 22kda form is the one used in synthetic GH and is 191 amino acids long.
The 20kda form is released naturally w/ 22kda. 20kda is identical however 15 amino acids in the part of the chain that interacts w/ the prolactin receptor are missing.
In rats 20kda produces less edema and less diabetogenic effect. In addition it doesn't interact w/ prolactin binding protein and has other characteristics a bit unique. In humans it is less clear if the side effects are less w/ 20kda then 22kda.
So using GHRH/GHRP to evoke a natural GH pulse means you get a blend of GHs (one of which is less diabetogenic).
That may be one reason.
All of the anecdotal feedback that I have received from diabetics tells me that the effect on blood sugar is less on the peptides then it is on synthetic GH.