[Buildbot] #2884: The Real Benefits Of GMAX Muscle Supplement And Role Of IGF-1 Skeleton Muscle

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#2884: The Real Benefits Of GMAX Muscle Supplement And Role Of IGF-1 Skeleton
Muscle
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Reporter:  jani11       |      Owner:  Dr. William
    Type:  enhancement  |     Status:  new
Priority:  minor        |  Milestone:  undecided
 Version:  0.8.9        |   Keywords:  GMAX
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 The role of IGF1 Akt pathway in adult skeletal muscle
 There is no doubt that IGF1 is an important regulator of muscle mass
 during '''GMAX Muscle''' development, due to its effect on proliferation
 and differentiation of myogenic cells. Regarding the role of IGF1 in adult
 skeletal muscle, several studies have shown that IGF1 can cause
 hypertrophy and atrophy of the unit. In adult rats, local infusion of
 recombinant IGF1 results in muscle hypertrophy and plasmid-mediated gene
 transfer of IGF1 prevents muscle atrophy induced by corticosteroids. In
 adult mice, virus-mediated gene transfer results IGF1 in muscle
 hypertrophy and prevents aging-dependent loss of muscle mass and strength.
 However, it is unclear whether IGF-1 is involved in mediating the effects
 of stress on adult muscle. Excess IGF1 in skeletal muscle of transgenic
 mice did not prevent muscle atrophy caused by unloading, although
 transgenic expression of IGF1 was reduced discharge in these experiments.
 Hypertrophy also unchanged in transgenic mice overexpression of dominant-
 negative form of IGF1 receptor overload, although the interpretation of
 this model is complicated by the double effect of the transgene on both
 insulin and IGF1 signaling. Ways mediate the effect of unloading and
 reloading the muscle were identified, and, as mentioned above, it is
 possible that Akt-mTOR way involved or integrin-ILK or by direct effects
 on MRM.

 The role of IGF1 and downstream effectors of adult skeletal muscle can not
 be determined using conventional knockout and transgenic approaches, since
 developing muscles have greater ductility than in adult muscle, so
 compensating devices can take place in response the gene overexpression or
 ablation is not visible when a genetic disturbance induced in adult
 animals. This may explain the lack of certain muscle phenotype knockout
 models, for example, the knock-out PI3K and PDK1. Other models knockout
 cause maladaptive changes that lead to muscular dystrophy, atrophy not
 like that seen in models of mTOR and Raptor-offs. Understanding the
 effects of genetic perturbations in adults rather than develop muscles is
 particularly important for the identification of therapeutic targets and
 design countermeasures to prevent muscle atrophy. To obtain useful
 information on this issue, it is necessary to use methods of transgenic
 inducible, the transgenic overexpression or gene knockout induced in adult
 animals. However, to our knowledge, a model of induction is the only act
 of inducing model developed so far to study IGF1 Akt pathway. Moreover,
 the in vivo transfection procedure can be used to study the effects of
 overexpression of the transgene or gene knockdown by RNAi in adult muscle.
 '''gmaxreclameaqui.com'''

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