Please Scroll Down to See Forums Below
S
satchboogie
Guest
this website is dedicate do IGF-1 only..
come check it out and contribue...
www.getIGF.com
come check it out and contribue...
www.getIGF.com
Last edited:
Baywatch69
New member
Great idea, I'm looking to give IGF a run very soon, Added that site to my bookmarks, sure it will come in handy 
Trying to find out the potential sides before I start, dont really seem to be many, the cancer link scares me
Trying to find out the potential sides before I start, dont really seem to be many, the cancer link scares me
psychedout
New member
Firstly, IGF may extend the lifespan of humans, if you believe the results from rats can be generalized.
IGF-1 receptor regulates lifespan and resistance to oxidative stress in miceMartin Holzenberger1, Joëlle Dupont2, Bertrand Ducos1, Patricia Leneuve1, Alain Géloën3, Patrick C. Even4, Pascale Cervera5 and Yves Le Bouc1
Top of pageStudies in invertebrates have led to the identification of a number of genes that regulate lifespan, some of which encode components of the insulin or insulin-like signalling pathways1, 2, 3. Examples include the related tyrosine kinase receptors InR (Drosophila melanogaster) and DAF-2 (Caenorhabditis elegans) that are homologues of the mammalian insulin-like growth factor type 1 receptor (IGF-1R). To investigate whether IGF-1R also controls longevity in mammals, we inactivated the IGF-1R gene in mice (Igf1r). Here, using heterozygous knockout mice because null mutants are not viable, we report that Igf1r+/- mice live on average 26% longer than their wild-type littermates (P < 0.02). Female Igf1r+/- mice live 33% longer than wild-type females (P < 0.001), whereas the equivalent male mice show an increase in lifespan of 16%, which is not statistically significant. Long-lived Igf1r+/- mice do not develop dwarfism, their energy metabolism is normal, and their nutrient uptake, physical activity, fertility and reproduction are unaffected. The Igf1r+/- mice display greater resistance to oxidative stress, a known determinant of ageing. These results indicate that the IGF-1 receptor may be a central regulator of mammalian lifespan.
IGF-1 receptor regulates lifespan and resistance to oxidative stress in miceMartin Holzenberger1, Joëlle Dupont2, Bertrand Ducos1, Patricia Leneuve1, Alain Géloën3, Patrick C. Even4, Pascale Cervera5 and Yves Le Bouc1
Top of pageStudies in invertebrates have led to the identification of a number of genes that regulate lifespan, some of which encode components of the insulin or insulin-like signalling pathways1, 2, 3. Examples include the related tyrosine kinase receptors InR (Drosophila melanogaster) and DAF-2 (Caenorhabditis elegans) that are homologues of the mammalian insulin-like growth factor type 1 receptor (IGF-1R). To investigate whether IGF-1R also controls longevity in mammals, we inactivated the IGF-1R gene in mice (Igf1r). Here, using heterozygous knockout mice because null mutants are not viable, we report that Igf1r+/- mice live on average 26% longer than their wild-type littermates (P < 0.02). Female Igf1r+/- mice live 33% longer than wild-type females (P < 0.001), whereas the equivalent male mice show an increase in lifespan of 16%, which is not statistically significant. Long-lived Igf1r+/- mice do not develop dwarfism, their energy metabolism is normal, and their nutrient uptake, physical activity, fertility and reproduction are unaffected. The Igf1r+/- mice display greater resistance to oxidative stress, a known determinant of ageing. These results indicate that the IGF-1 receptor may be a central regulator of mammalian lifespan.
psychedout
New member
IGF-1 induces skeletal myocyte hypertrophy through calcineurin in association with GATA-2 and NF-ATc1
ANTONIO MUSARÒ*, KARL J. A. MCCULLAGH*, FRANCISCO J. NAYA†, ERIC N. OLSON† & NADIA ROSENTHAL*
* Cardiovascular Research Center, Massachusetts General HospitalEast, 149 13th Street, Charlestown, Massachusetts 02129, USA
† Department of Molecular Biology and Oncology, the University of Texas Southwestern Medical Center, 6000 Harry Hines Blvd, Dallas, Texas 75225, USA
Localized synthesis of insulin-like growth factors (IGFs) has been broadly implicated in skeletal muscle growth, hypertrophy and regeneration. Virally delivered IGF-1 genes induce local skeletal muscle hypertrophy and attenuate age-related skeletal muscle atrophy, restoring and improving muscle mass and strength in mice. Here we show that the molecular pathways underlying the hypertrophic action of IGF-1 in skeletal muscle are similar to those responsible for cardiac hypertrophy. Transfected IGF-1 gene expression in postmitotic skeletal myocytes activates calcineurin-mediated calcium signalling by inducing calcineurin transcripts and nuclear localization of calcineurin protein. Expression of activated calcineurin mimics the effects of IGF-1, whereas expression of a dominant-negative calcineurin mutant or addition of cyclosporin, a calcineurin inhibitor, represses myocyte differentiation and hypertrophy. Either IGF-1 or activated calcineurin induces expression of the transcription factor GATA-2, which accumulates in a subset of myocyte nuclei, where it associates with calcineurin and a specific dephosphorylated isoform of the transcription factor NF-ATc1. Thus, IGF-1 induces calcineurin-mediated signalling and activation of GATA-2, a marker of skeletal muscle hypertrophy, which cooperates with selected NF-ATc isoforms to activate gene expression programs.
ANTONIO MUSARÒ*, KARL J. A. MCCULLAGH*, FRANCISCO J. NAYA†, ERIC N. OLSON† & NADIA ROSENTHAL*
* Cardiovascular Research Center, Massachusetts General HospitalEast, 149 13th Street, Charlestown, Massachusetts 02129, USA
† Department of Molecular Biology and Oncology, the University of Texas Southwestern Medical Center, 6000 Harry Hines Blvd, Dallas, Texas 75225, USA
Localized synthesis of insulin-like growth factors (IGFs) has been broadly implicated in skeletal muscle growth, hypertrophy and regeneration. Virally delivered IGF-1 genes induce local skeletal muscle hypertrophy and attenuate age-related skeletal muscle atrophy, restoring and improving muscle mass and strength in mice. Here we show that the molecular pathways underlying the hypertrophic action of IGF-1 in skeletal muscle are similar to those responsible for cardiac hypertrophy. Transfected IGF-1 gene expression in postmitotic skeletal myocytes activates calcineurin-mediated calcium signalling by inducing calcineurin transcripts and nuclear localization of calcineurin protein. Expression of activated calcineurin mimics the effects of IGF-1, whereas expression of a dominant-negative calcineurin mutant or addition of cyclosporin, a calcineurin inhibitor, represses myocyte differentiation and hypertrophy. Either IGF-1 or activated calcineurin induces expression of the transcription factor GATA-2, which accumulates in a subset of myocyte nuclei, where it associates with calcineurin and a specific dephosphorylated isoform of the transcription factor NF-ATc1. Thus, IGF-1 induces calcineurin-mediated signalling and activation of GATA-2, a marker of skeletal muscle hypertrophy, which cooperates with selected NF-ATc isoforms to activate gene expression programs.
psychedout
New member
Here is some more. I am aware some of this literature may have to be stretched to apply to bodybuilders, but most of the literature regarding us is.
Muscle Protein Catabolism After Severe Burn: Effects of IGF-1/IGFBP-3 Treatment.
Annals of Surgery. 229(5):713, May 1999.
Herndon, David N. MD; Ramzy, Peter I. MD; DebRoy, Meelie A. MD; Zheng, Ming MD; Ferrando, Arny A. PhD; Chinkes, David L. PhD; Barret, Juan P. MD; Wolfe, Robert R. PhD; Wolf, Steven E. MD
Abstract:
Objective: To determine the effects of recombinant human insulin-like growth factor-1 (IGF-1) complexed with its principal binding protein, IGFBP-3, on skeletal muscle metabolism in severely burned children.
Summary Background Data: Severe burns are associated with a persistent hypermetabolic response characterized by hyperdynamic circulation and severe muscle catabolism and wasting. Previous studies showed that nutritional support and pharmacologic intervention with anabolic agents such as growth hormone and insulin abrogated muscle wasting and improved net protein synthesis in the severely burned. The use of these agents, however, has several adverse side effects. A new combination of IGF-1 and IGFBP-3 is now available for clinical study.
Methods: Twenty-nine severely burned children were prospectively studied before and after treatment with 0.5, 1, 2, or 4 mg/kg/day IGF-1/IGFBP-3 to determine net balance of protein across the leg, muscle protein fractional synthetic rates, and glucose metabolism. Another group was studied in a similar fashion without IGF-1/IGFBP-3 treatment as time controls.
Results: Seventeen of 29 children were catabolic before starting treatment. The infusion of 1.0 mg/kg/day IGF-1/IGFBP-3 increased serum IGF-1, which did not further increase with 2.0 and 4.0 mg/kg/day. IGF-1/IGFBP-3 treatment at 1 to 4 mg/kg/day improved net protein balance and increased muscle protein fractional synthetic rates. This effect was more pronounced in catabolic children. IGF-1/IGFBP-3 did not affect glucose uptake across the leg or change substrate utilization.
Conclusions: IGF-1/IGFBP-3 at doses of 1 to 4 mg/kg/day attenuates catabolism in catabolic burned children with negligible clinical side effects.
Muscle Protein Catabolism After Severe Burn: Effects of IGF-1/IGFBP-3 Treatment.
Annals of Surgery. 229(5):713, May 1999.
Herndon, David N. MD; Ramzy, Peter I. MD; DebRoy, Meelie A. MD; Zheng, Ming MD; Ferrando, Arny A. PhD; Chinkes, David L. PhD; Barret, Juan P. MD; Wolfe, Robert R. PhD; Wolf, Steven E. MD
Abstract:
Objective: To determine the effects of recombinant human insulin-like growth factor-1 (IGF-1) complexed with its principal binding protein, IGFBP-3, on skeletal muscle metabolism in severely burned children.
Summary Background Data: Severe burns are associated with a persistent hypermetabolic response characterized by hyperdynamic circulation and severe muscle catabolism and wasting. Previous studies showed that nutritional support and pharmacologic intervention with anabolic agents such as growth hormone and insulin abrogated muscle wasting and improved net protein synthesis in the severely burned. The use of these agents, however, has several adverse side effects. A new combination of IGF-1 and IGFBP-3 is now available for clinical study.
Methods: Twenty-nine severely burned children were prospectively studied before and after treatment with 0.5, 1, 2, or 4 mg/kg/day IGF-1/IGFBP-3 to determine net balance of protein across the leg, muscle protein fractional synthetic rates, and glucose metabolism. Another group was studied in a similar fashion without IGF-1/IGFBP-3 treatment as time controls.
Results: Seventeen of 29 children were catabolic before starting treatment. The infusion of 1.0 mg/kg/day IGF-1/IGFBP-3 increased serum IGF-1, which did not further increase with 2.0 and 4.0 mg/kg/day. IGF-1/IGFBP-3 treatment at 1 to 4 mg/kg/day improved net protein balance and increased muscle protein fractional synthetic rates. This effect was more pronounced in catabolic children. IGF-1/IGFBP-3 did not affect glucose uptake across the leg or change substrate utilization.
Conclusions: IGF-1/IGFBP-3 at doses of 1 to 4 mg/kg/day attenuates catabolism in catabolic burned children with negligible clinical side effects.
psychedout
New member
IGF-I stimulates muscle growth by suppressing protein breakdown and expression of atrophy-related ubiquitin ligases, atrogin-1 and MuRF1.
This is a pretty big one, a little to big to cut and post, but the direct link is:
http://ajpendo.physiology.org/cgi/content/full/287/4/E591
Expression, Regulation, and Function of IGF-1, IGF-1R, and IGF-1 Binding Proteins in Blood Vessels
Again, a little large, but here is the link.
http://atvb.ahajournals.org/cgi/content/full/24/3/435
Beneficial effects of GH/IGF-1 on skeletal muscle atrophy and function in experimental heart failure
Third one. Apparently it can reduce your chance of CHF. I think that stands for cardiovascular heart failure. My interpretation may be wrong though.
http://intl-ajpcell.physiology.org/cgi/content/full/286/1/C138
This is a pretty big one, a little to big to cut and post, but the direct link is:
http://ajpendo.physiology.org/cgi/content/full/287/4/E591
Expression, Regulation, and Function of IGF-1, IGF-1R, and IGF-1 Binding Proteins in Blood Vessels
Again, a little large, but here is the link.
http://atvb.ahajournals.org/cgi/content/full/24/3/435
Beneficial effects of GH/IGF-1 on skeletal muscle atrophy and function in experimental heart failure
Third one. Apparently it can reduce your chance of CHF. I think that stands for cardiovascular heart failure. My interpretation may be wrong though.
http://intl-ajpcell.physiology.org/cgi/content/full/286/1/C138
Güclü_oglan
New member
i've ran IGF-1 from pharmacies twice lately (both from sweden and from turkey) and i wouldn't advice you bros to do it unless very rich and won't bother a loss at a grand for a good cycle of IGF
got hungrier and i got more water in my muscles but nothing more
remember there are many theories of that IGF-1 can contribute to development of cancer
i'm skeptical but try it out and see if it works for you
got hungrier and i got more water in my muscles but nothing more
remember there are many theories of that IGF-1 can contribute to development of cancer
i'm skeptical but try it out and see if it works for you
Similar threads
