Muscle-specific inactivation of the IGF-I receptor induces compensatory hyperplasia

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    Muscle-specific inactivation of the IGF-I receptor induces compensatory hyperplasia


    Muscle-specific inactivation of the IGF-I receptor induces compensatory hyperplasia in skeletal muscle
    Ana M. FernŠndez1, JoŽlle Dupont1, Roger P. Farrar2, Sukho Lee2, Bethel Stannard1 and Derek Le Roith1

    1 Clinical Endocrinology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA
    2 Department of Kinesiology, University of Texas at Austin, Austin, Texas, USA

    Address correspondence to: Derek Le Roith, Molecular and Cellular Physiology Section, Clinical Endocrinology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 9000 Rockville Pike, Building 10, Room 8D12, Bethesda, Maryland 20892-1758, USA. Phone: (301) 496-8090; Fax: (301) 480-4386; E-mail: derek@helix.nih.gov.

    Received for publication June 13, 2001, and accepted in revised form December 28, 2001.

    During the development of skeletal muscle, myoblasts withdraw from the cell cycle and differentiate into myotubes. The insulin-like growth factors IGF-I and IGF-II, through their cognate tyrosine kinase receptor (IGF-I receptor), are known to play a role in this process. After withdrawal of myoblasts from the cell cycle, IGF-I promotes muscle differentiation by inducing the expression or activity of myogenic regulatory factors (MyoD, myogenin) and effectors (p21). However, little is known about the intracellular mechanisms by which the IGF-I system regulates these factors during the process of myogenesis. Here we show that MKR mice, which express a dominant negative IGF-I receptor specifically in skeletal muscle, have marked muscle hypoplasia from birth to 3 weeks of age. This hypoplasia occurs concomitantly with a decrease in ERK immunoreactivity levels and decreases in MyoD and myogenin expression. BrdU immunocytochemistry showed a compensatory hyperplasia as MKR mice grew to adulthood. Interestingly, hyperplasia occurred concomitantly with an increase in p38, MyoD, myogenin, and p21 immunoreactivity levels, as well as a decrease in Twist levels. These findings suggest that regulation of these cellular elements by IGF-I may play a role in the development and differentiation of skeletal muscle in vivo.

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    so basically if this holds true in vivo in humans, one that would want to induce hyperplasia would want to keep running 1gf-i past the point were most stop seeing noticeable results? the results most are seeing from this would be from a boatload of the daosage being spliced towards MGF and hypertrophy, and after sometime this route gets downregulated? ~4weeks?
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    Interesting ... I'd like to hear more.
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    Re: Muscle-specific inactivation of the IGF-I receptor induces compensatory hyperplas


    Quote Originally Posted by SprtNvolcoM
    Interesting ... I'd like to hear more.
    I am doing my best. Hard as hell to find studies on skeletal muscle hyperplasia in humans. There have been a lot of studies on them in mammals in general and they actually see considerable hyperplasia in them (even more in avian species) without growth factors but on a lot of studies done on humans they found no increase in fiber number. I am researching my ass off though.
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    Hey man good work just the same. I tried to rep you but apprently I must spread the love. Keep up the good work though. Much appreciated.
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    Quote Originally Posted by SprtNvolcoM
    Hey man good work just the same. I tried to rep you but apprently I must spread the love. Keep up the good work though. Much appreciated.
    Apparently, LMD is hordeing all the Love- rightfully so.



    Nice artical!!!!
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    any more thoughts about this study?
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    Re: Muscle-specific inactivation of the IGF-I receptor induces compensatory hyperplas


    Quote Originally Posted by 2slow
    any more thoughts about this study?
    Not really too much involved with it, meaning you can't really read too much more into it. I mean it is basically saying that MyoD and other expression factors are correlated with muscle cell hyperplasia and that IGF-1 increases MyoD expression, therefore, they are saying that IGF-1 promotes muscle cell hyperplasia.

    But as I stated before, there are barely ANY studies done on muscle cell hyperplasia in humans caused by growth factors. Some of them point to no and some point to yes.
  

  
 

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