Finally research had been done that shows us exactly how effective the IGF we use to inj is compared to the gene doping research that most of the studies boasting IGF claims are based on. This first study compared directly the IGF-gene tranfer to adminstering the IGF-I peptide systemically. Gene transfer was superior by no surprise, but what is good news is that IGF-I hastened functional recovery, regardless of the route of IGF-I administration. The systemic IGF took a whole 7 days to give the same muscle recovery as the gene doping did, (21 dasy compared to 14). This is because it is easier for gene doping to result in the intracellular signaling.
Below is another study that shows that systemic IGF is effective at repairing muscles in mice with MD.
Comparative evaluation of IGF-I gene transfer and IGF-I protein administration for enhancing skeletal muscle regeneration after injury.
· Schertzer JD,
· Lynch GS.
1Basic and Clinical Myology Laboratory, Department of Physiology, The University of Melbourne, Victoria, Australia.
Developing methodologies to enhance skeletal muscle regeneration and hasten the restoration of muscle function has important implications for minimizing disability after injury and for treating muscle diseases such as Duchenne muscular dystrophy. Although delivery of various growth factors, such as insulin-like growth factor-I (IGF-I), have proved successful in promoting skeletal muscle regeneration after injury, no study has compared the efficacy of different delivery methods directly. We compared the efficacy of systemic delivery of recombinant IGF-I protein via mini-osmotic pump ( approximately 1.5 mg/kg/day) with a single electrotransfer-assisted plasmid-based gene transfer, to hasten functional repair of mouse tibialis anterior muscles after myotoxic injury. The relative efficacy of each method was assessed at 7, 21 and 28 days post-injury. Our findings indicate that IGF-I hastened functional recovery, regardless of the route of IGF-I administration. However, gene transfer of IGF-I was superior to systemic protein administration because in the regenerating muscle, this delivery method increased IGF-I levels, activated intracellular signals (Akt phosphorylation), induced a greater magnitude of myofiber hypertrophy and hastened functional recovery at an earlier time point (14 days) after injury than did protein administration (21 days). Thus, the relative efficacy of different modes of delivery is an important consideration when assessing the therapeutic potential of various proteins for treating muscle injuries and skeletal muscle diseases.Gene Therapy advance online publication, 27 July 2006; doi:10.1038/sj.gt.3302817.
Systemic administration of IGF-I enhances oxidative status and reduces contraction-induced injury in skeletal muscles of mdx dystrophic mice.
* Schertzer JD,
* Ryall JG,
* Lynch GS.
Dept. of Physiology, The Univ. of Melbourne, Victoria 3010, Australia.
gsl@unimelb.edu.au).
The absence of dystrophin and resultant disruption of the dystrophin glycoprotein complex renders skeletal muscles of dystrophic patients and dystrophic mdx mice susceptible to contraction-induced injury. Strategies to reduce contraction-induced injury are of critical importance, because this mode of damage contributes to the etiology of myofiber breakdown in the dystrophic pathology. Transgenic overexpression of insulin-like growth factor-I (IGF-I) causes myofiber hypertrophy, increases force production, and can improve the dystrophic pathology in mdx mice. In contrast, the predominant effect of continuous exogenous administration of IGF-I to mdx mice at a low dose (1.0-1.5 mg.kg(-1).day(-1)) is a shift in muscle phenotype from fast glycolytic toward a more oxidative, fatigue-resistant, slow muscle without alterations in myofiber cross-sectional area, muscle mass, or maximum force-producing capacity. We found that exogenous administration of IGF-I to mdx mice increased myofiber succinate dehydrogenase activity, shifted the overall myosin heavy chain isoform composition toward a slower phenotype, and, most importantly, reduced contraction-induced damage in tibialis anterior muscles. The deficit in force-producing capacity after two damaging lengthening contractions was reduced significantly in tibialis anterior muscles of IGF-I-treated (53 +/- 4%) compared with untreated mdx mice (70 +/- 5%, P < 0.05). The results provide further evidence that IGF-I administration can enhance the functional properties of dystrophic skeletal muscle and, compared with results in transgenic mice or virus-mediated overexpression, highlight the disparities in different models of endocrine factor delivery.
