Buy Needles And Syringes With No Prescription
M4B Store Banner
intex
Riptropin Store banner
Generation X Bodybuilding Forum
Buy Needles And Syringes With No Prescription
Buy Needles And Syringes With No Prescription
Mysupps Store Banner
IP Gear Store Banner
PM-Ace-Labs
Ganabol Store Banner
Spend $100 and get bonus needles free at sterile syringes
Professional Muscle Store open now
sunrise2
PHARMAHGH1
kinglab
ganabol2
Professional Muscle Store open now
over 5000 supplements on sale at professional muscle store
azteca
granabolic1
napsgear-210x65
advertise1
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
ashp210
UGFREAK-banner-PM
esquel
YMSGIF210x65-Banner
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store
over 5000 supplements on sale at professional muscle store

Does MGF inlarge the digestive tract?

Ok no one has replied to this one, but Ive concluded it does because it acts as IGF out side of the cell.
 
Ok no one has replied to this one, but Ive concluded it does because it acts as IGF out side of the cell.

MGF only exists in skeletal muscle. It's primary purpose is not making cells bigger, it's building new muscle cell nuclei. This is what it was designed for and one of the reasons it's promising although I have not seen anyone who says they were amazed at the results. As I've heard it's best used as a supplement to IGF-1R3.
 
Does MGF inlarge the digestive tract?

no it doesnt. igf receptors are present in digestive tract so IGF travelling in the blood will naturally be drawn to it. MGf receptors dont exist.

Put it in the correct forum next time and people will answer
 
Actually dat has said that mgf receptors don't exist and it is true. Only igf receptors exist and I believe that mgf is used by the igf receptors. Remember, mgf is a form of igf. Also, the reason why people don't rave of mgf results is because they don't use a high enough dose all at once into the muscles. IMO, a very high dose needs to be administered after workout to see results.
 
I am aware of where MGF comes from. Unless datbtrue is working alongside one of the few researchers in the world that is publishing data on MGF, I would be very suspicious of his statements. Peptides generally have receptors (this is what nature uses them for), and it would be very unlikely that MGF transduced signals through the IGF-1 receptor due to their vastly different primary sequence and secondary structures. Hence something else is probably at play.

It is also important to remember that MGF was only discovered in the past 10 years and not a lot of work has been done examining its biology. IGF-1 has been studied for much longer.

But to exemplify the lack of knowledge the field has on this hormone, look towards this recent publication that merely examines to see if MGF acts through the same pathways as IGF-1:

Mol Med. 2009 Mar 19.
IGF-1 Expression in Infarcted Myocardium and MGF E Peptide Actions on Rat Cardiomyocytes, In Vitro.
Stavropoulou A, Halapas A, Sourla A, Philippou A, Papageorgiou E, Papalois A, Koutsilieris M.

Department of Experimental Physiology, MedicalSchool, National Kapodistrian University of Athens, Goudi-Athens, Greece.

Insulin-like growth factor-1 (IGF-1) expression is implicated in myocardial pathophysiology and two IGF-1 mRNA splice variants have been detected in rodents, namely the IGF-1Ea and the mechano-growth factor (MGF). Consequently, we have investigated the expression pattern of the IGF-1 gene transcripts in rat myocardium after left anterior descending coronary artery ligation-induced myocardial infarction (1hr up to 8wks). In addition, we characterized IGF-1 and MGF E peptide action and their respective signaling in H9C2 myocardial-like cells, in vitro. IGF-1Ea and MGF expression were significantly increased, both at transcriptional and translational level, during the late post-infarction period (4wks and 8wks) in infracted rat myocardium. Measurements of serum IGF-1 levels in infracted rats were initially decreased (24hr up to 1wk) but remained unaltered throughout the late experimental phase (4wks to 8wks) as compared to this of sham-operated rats. Furthermore, specific anti-IGF-1R neutralizing antibody failed to block the synthetic MGF E peptide action while it blocked completely IGF-1 action on the proliferation of H9C2 cells. Moreover, this synthetic MGF E peptide did not activate Akt phosphorylation while it activated ERK1/2 in H9C2 rat myocardial cells. These data support the role of IGF-1 expression in myocardial repair process and suggest that synthetic MGF E peptide actions are mediated possibly via an IGF-1R independent pathway in rat myocardial cells, as suggested by our in vitro experiments.

-------------------------------

Notice they say no Akt phosphorylation occurred (a hallmark of IGF-1 signaling) whereas ERK1/2 were activated. ERK1/2 activation would suggest the activity of a yet-to-be-identified GPCR.
 
Last edited:
I am aware of where MGF comes from. Unless datbtrue is working alongside one of the few researchers in the world that is publishing data on MGF, I would be very suspicious of his statements. Peptides generally have receptors (this is what nature uses them for), and it would be very unlikely that MGF transduced signals through the IGF-1 receptor due to their vastly different primary sequence and secondary structures. Hence something else is probably at play.

It is also important to remember that MGF was only discovered in the past 10 years and not a lot of work has been done examining its biology. IGF-1 has been studied for much longer.

But to exemplify the lack of knowledge the field has on this hormone, look towards this recent publication that merely examines to see if MGF acts through the same pathways as IGF-1:

Mol Med. 2009 Mar 19.
IGF-1 Expression in Infarcted Myocardium and MGF E Peptide Actions on Rat Cardiomyocytes, In Vitro.
Stavropoulou A, Halapas A, Sourla A, Philippou A, Papageorgiou E, Papalois A, Koutsilieris M.

Department of Experimental Physiology, MedicalSchool, National Kapodistrian University of Athens, Goudi-Athens, Greece.

Insulin-like growth factor-1 (IGF-1) expression is implicated in myocardial pathophysiology and two IGF-1 mRNA splice variants have been detected in rodents, namely the IGF-1Ea and the mechano-growth factor (MGF). Consequently, we have investigated the expression pattern of the IGF-1 gene transcripts in rat myocardium after left anterior descending coronary artery ligation-induced myocardial infarction (1hr up to 8wks). In addition, we characterized IGF-1 and MGF E peptide action and their respective signaling in H9C2 myocardial-like cells, in vitro. IGF-1Ea and MGF expression were significantly increased, both at transcriptional and translational level, during the late post-infarction period (4wks and 8wks) in infracted rat myocardium. Measurements of serum IGF-1 levels in infracted rats were initially decreased (24hr up to 1wk) but remained unaltered throughout the late experimental phase (4wks to 8wks) as compared to this of sham-operated rats. Furthermore, specific anti-IGF-1R neutralizing antibody failed to block the synthetic MGF E peptide action while it blocked completely IGF-1 action on the proliferation of H9C2 cells. Moreover, this synthetic MGF E peptide did not activate Akt phosphorylation while it activated ERK1/2 in H9C2 rat myocardial cells. These data support the role of IGF-1 expression in myocardial repair process and suggest that synthetic MGF E peptide actions are mediated possibly via an IGF-1R independent pathway in rat myocardial cells, as suggested by our in vitro experiments.

-------------------------------

Notice they say no Akt phosphorylation occurred (a hallmark of IGF-1 signaling) whereas ERK1/2 were activated. ERK1/2 activation would suggest the activity of a yet-to-be-identified GPCR.

Ok perhaps my bad on the non existence but it is yet to be found. when tests have been done with IGF and MGf being run concurrently, they haven't competed for receptors despite the fact they both use the same pathway.
 
when tests have been done with IGF and MGf being run concurrently, they haven't competed for receptors despite the fact they both use the same pathway.

What tests are you referring to?

Given what this publication states, there could be subtle differences in what IGF-1 and MGF are able to achieve in terms of muscle growth. The fact that MGF does not induce Akt phosphorylation but rather ERK1/2 may signal that either both are needed for optimal muscle recovery or that they instill different biological processes all together, and pending what sort of trauma is provided to the muscle, you may need/want more of one or the other or both to recover. MGF is a very interesting peptide though, there should be a lot more to come from it in the future.

FYI: Paper full text is available for free: http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=2656994&blobtype=pdf
 
What tests are you referring to?

Given what this publication states, there could be subtle differences in what IGF-1 and MGF are able to achieve in terms of muscle growth. The fact that MGF does not induce Akt phosphorylation but rather ERK1/2 may signal that either both are needed for optimal muscle recovery or that they instill different biological processes all together, and pending what sort of trauma is provided to the muscle, you may need/want more of one or the other or both to recover. MGF is a very interesting peptide though, there should be a lot more to come from it in the future.

FYI: Paper full text is available for free: http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=2656994&blobtype=pdf

trying to find it now for you.

I've got this in my notes section in outlook but cant find the site i nicked it from. it just outlines that igf and mgf wont compete for receptors. if i can find the rest i'll post it up. saying that i think Dat has posted stuff on here about it

The physiological function of MGF was studied using an in vitro cell model. Unlike IGF-I, the distinct E domain of MGF inhibits terminal differentiation whilst increasing myoblast proliferation. Blocking the IGF-I receptor with a specific antibody indicated that the function of MGF E domain is mediated via a different receptor. The results provide a basis for localized tissue adaptation and helps explain why loss of muscle mass occurs in the elderly and in dystrophic muscle in which MGF production is markedly affected (Yang SY, Goldspink G., 2002, p. 156-60).
 
Last edited:

Staff online

  • rAJJIN
    Moderator / FOUNDING Member

Forum statistics

Total page views
558,027,718
Threads
135,751
Messages
2,768,522
Members
160,339
Latest member
Dann828
NapsGear
HGH Power Store email banner
your-raws
Prowrist straps store banner
infinity
FLASHING-BOTTOM-BANNER-210x131
raws
Savage Labs Store email
Syntherol Site Enhancing Oil Synthol
aqpharma
yourmuscleshop210x131
hulabs
ezgif-com-resize-2-1
MA Research Chem store banner
MA Supps Store Banner
volartek
Keytech banner
musclechem
Godbullraw-bottom-banner
Injection Instructions for beginners
Knight Labs store email banner
3
ashp131
YMS-210x131-V02
Back
Top