I have been reading up a lot on IGF and wanted to know what exactly it is used for?? I know that it is insulin and is very powerful. I have read that it helps shuddle nutrients, helps with muscle growth, gives you extra endurance and energy. Who here uses IGF and why do you use it?
Question about IGF???
- Thread starter ludakris9
- Start date
cubanojoe
New member
It is not insulin, far from it.
Yes it does shuttle nutrients into the cell like insulin but when you take HGH for example your liver will produce IGF-1 and IGF-2, IGF-1 being what we want.
It will cause your muscle cells to divide and make new ones which is what we want since steroid use only makes our muscle cells bigger and not new ones.
Yes it does shuttle nutrients into the cell like insulin but when you take HGH for example your liver will produce IGF-1 and IGF-2, IGF-1 being what we want.
It will cause your muscle cells to divide and make new ones which is what we want since steroid use only makes our muscle cells bigger and not new ones.
Bruce Banner
G.F.H.
cubanojoe said:
This is quite controversiall and not a fact from what I know.
/Bruce
BigRonWannabee
New member
Ive seen evidence that it can help recruit satellite cells and turn them into functional hypertrophy capable cells.
Bruce Banner
G.F.H.
cubanojoe said:
Well, there is different isoforms of IGF-1. I think IGF-1 localy produced in muscle cells is important for muscle growth, not liver produced.
/Bruce
Bruce Banner
G.F.H.
ludakris9 said:
I have used insulin quite a bit actually.
Have not done IGF-1 because I do not think it builds muscle at all, and it's very expensive. Would like to try however.
/Bruce
JohnnyB
Community Veteran
IGF-1=Insulin-Like GrowthFactor, it has insulin like properties, with Growth factor properties as well. So you could say it's like slin, but like HGH too. Because of those 2 properties, you can gain muscle and lose fat while using LR3 IGF-1, LR3 has an extended half-life, of around 6 hours. hIGF-1 as a half-life of 10-20 minutes.
JohnnyB
JohnnyB
Bruce Banner
G.F.H.
A bit technical but hey, it's an explanation how IGF-1 works.
IGF-1 stimulates muscle growth by suppressing protein breakdown and expression of atrophy-related ubiquitin-ligases, atrogin-1 and MuRF1
Jennifer M. Sacheck1, Akira Ohtsuka2, S. Christine McLary1, and Alfred L. Goldberg1*
1 Department of Cell Biology, Harvard Medical School, Boston, MA, USA
2 Department of Biochemical Science and Technology, Kagoshima University, Korimoto, Kagoshima, Japan
* To whom correspondence should be addressed. E-mail: alfred_goldberg@hms.harvard.edu.
Muscle atrophy results primarily from accelerated protein degradation and is associated with increased expression of two muscle-specific ubiquitin-ligases, atrogin-1 and MuRF1. Glucocorticoids are essential for many types of muscle atrophy, and their effects are opposite to IGF-1 and insulin, which promote growth. In myotubes, dexamethasone inhibited growth and enhanced the breakdown of long-lived cell proteins, especially of myofibrillar proteins (as measured by 3-methylhistidine release), while also increasing atrogin-1 and MuRF1 mRNA. Conversely, IGF-1 suppressed protein degradation and prevented the dexamethasone-induced increase in proteolysis. IGF-1 rapidly reduced atrogin-1 expression within one hour by blocking mRNA synthesis without affecting mRNA degradation, while IGF-1 decreased MuRF1 mRNA slowly. IGF-1 and insulin also blocked the dexamethasone induction of these ubiquitin-ligases and several other atrophy-related genes ("atrogenes"). The changes in overall proteolysis with dexamethasone and IGF-1 correlated tightly with the changes in atrogin-1 mRNA content, but not with the changes in MuRF1 mRNA. IGF-1 activates the PI3-kinase/Akt pathway and inhibition of this pathway (but not the calcineurin/NFAT or MEK/ERK pathways) increased proteolysis and atrogin-1 mRNA expression. Thus, an important component of growth stimulation by IGF-1, through the PI3-kinase/Akt pathway, is its ability to rapidly suppress transcription of the atrophy-related E3, atrogin-1, other atrogenes, and degradation of myofibrillar proteins.
MVH
/Bruce
IGF-1 stimulates muscle growth by suppressing protein breakdown and expression of atrophy-related ubiquitin-ligases, atrogin-1 and MuRF1
Jennifer M. Sacheck1, Akira Ohtsuka2, S. Christine McLary1, and Alfred L. Goldberg1*
1 Department of Cell Biology, Harvard Medical School, Boston, MA, USA
2 Department of Biochemical Science and Technology, Kagoshima University, Korimoto, Kagoshima, Japan
* To whom correspondence should be addressed. E-mail: alfred_goldberg@hms.harvard.edu.
Muscle atrophy results primarily from accelerated protein degradation and is associated with increased expression of two muscle-specific ubiquitin-ligases, atrogin-1 and MuRF1. Glucocorticoids are essential for many types of muscle atrophy, and their effects are opposite to IGF-1 and insulin, which promote growth. In myotubes, dexamethasone inhibited growth and enhanced the breakdown of long-lived cell proteins, especially of myofibrillar proteins (as measured by 3-methylhistidine release), while also increasing atrogin-1 and MuRF1 mRNA. Conversely, IGF-1 suppressed protein degradation and prevented the dexamethasone-induced increase in proteolysis. IGF-1 rapidly reduced atrogin-1 expression within one hour by blocking mRNA synthesis without affecting mRNA degradation, while IGF-1 decreased MuRF1 mRNA slowly. IGF-1 and insulin also blocked the dexamethasone induction of these ubiquitin-ligases and several other atrophy-related genes ("atrogenes"). The changes in overall proteolysis with dexamethasone and IGF-1 correlated tightly with the changes in atrogin-1 mRNA content, but not with the changes in MuRF1 mRNA. IGF-1 activates the PI3-kinase/Akt pathway and inhibition of this pathway (but not the calcineurin/NFAT or MEK/ERK pathways) increased proteolysis and atrogin-1 mRNA expression. Thus, an important component of growth stimulation by IGF-1, through the PI3-kinase/Akt pathway, is its ability to rapidly suppress transcription of the atrophy-related E3, atrogin-1, other atrogenes, and degradation of myofibrillar proteins.
MVH
/Bruce
oswaldosalcedo
New member
a lot of side effects, and modest results at 50-70mcg (LR3),
regard to IGF1 need bigger doses
regard to IGF1 need bigger doses
cubanojoe said:
Do you like IGF so far? Have you had any problems with it snice I have been told it is really dangerous,but you see to know how to regulated it so you will probally see good results from it. Let me know in a few weeks how you are doing with IGF.
Also bruce banner thanks for all the awesome info in your post bro.
I've been on it for about 2-3 weeks and I have put on 10-12 lbs (I'm on 1g Test undecanote) so the test is just kickin in. Was on Anavar (var) at 50mg Ed for the first 2 weeks. I have been doing 60-70mcg 3x a day. I like it so far, thought it would do more for fat loss. Anyway, no problems with IGF, get really good pumps from it though.
Similar threads
