MGF refers to mechano growth factor, a chemical that is capable of assisting the release of IG-1 in muscle tissue. This chemical is naturally released after periods of exercise or exertion in the body; synthesized versions of this chemical are designed as a means of understanding or mimicking this reaction in research. Scientists hope that a synthetic version of MGF can be created that will interact with stem and satellite cells throughout the anabolic process, to correct issues that stem from a lack of muscular growth.
When a muscle reaches mechanical overload IGF-1 is released and can be spliced in a variety of different ways, as needed by the body. Initially this will produce IGF-1Ec which is an MGF splice of this chemical. This allows any undamaged nuclei to be triggered, to grow new tissue via protein synthesis. This expression of MGF can lead the way for additional splice variants which are believed to be an anabolic mechanism used for an animal to grow new muscle.
The expression of mRNA in splice variants of IGF-1 and mechano growth factor were examined in tissue samples from skeletal muscle.
After exposing a variety of age groups to a rigorous exercise routine, samples were taken from the single legged knee extensor and a biopsy sample of quadriceps muscle on exercised legs.
These samples were checked for the natural presence of MGF and IGF-2 mRNA to determine the time necessary for these chemicals to appear.
Throughout the study period it did not appear as though a resting period affected the times necessary for these chemicals to begin work on the muscle tissue. Older subjects learnt that a larger amount of exercise was necessary for MGF to appear.
There did not appear to be isolation between young subjects and the composition of muscle when IGF isoforms appeared, following exercise.
There is presently no treatment for the economic and physical costs of an ischemic stroke, but IGF-1 may be able to assist with neuronal maintenance, to prevent this damage.
The neuronal maintenance abilities of chemicals spliced from MGF (IGF-1) in stabilized C-terminal or synthetic applications were investigated to determine if they could prevent or decrease acute ischemia-evoked neurogegeneration.
Sequence database analysis revealed that a high concentration of MGF in animals, such as gerbils, confirmed that this chemical splices in the liver. This produces a frame shift that allows mRNA to translate into an isoform.
PCR analysis shows that MGF mRNA in gerbil brains increases the expression of MGF. This is evident 3 hours after applications and can be seen for up to 72 hours.
IGF-1 expression has been expressed in two variants in rodents which implicates this chemical in myocardial pathophysiology.
Gene transcript expression patterns were investigated in rats for 108 weeks after they experienced a myocardial infarction. IGF-1Ea and MGF expressions were highly increased at translational and transcriptional levels.
Measurements toward the end of this study revealed that IGF-1 levels began to decrease but MGF levels remained high. MGF E peptides blocked the actions of IGF-1 and failed to activate Akt phosphorylation. This helped to activate myocardial repairs and suggests that MGF can be mediated with IGf-1R via an independent pathway, from those explored in in vitro experiments.
In rodents it was found that injecting MGF resulted in a 25 percent increase in their mean muscle fiber, in as little as three weeks. Applying IGF-1 alone took four months to produce a 15 percent increase of the same muscle tissue. It appears that young animals respond more effectively to these applications than those who have aged, which may account for some of this difference.