i found a study done on igf-1lr3, i think?

[flexshack]

http://ajpregu.physiology.org/cgi/co...rt/285/6/R1481

here it is. sorry i can't translate into english, but maybe someone else can? (einstein??) i just thought it might be useful in our quest for more knowledge on this stuff.

[einstein1905]

Extracellular signal-regulated kinase and phosphoinositol-3 kinase mediate IGF-1 induced proliferation of fetal sheep cardiomyocytes
Nathan C. Sundgren,1 George D. Giraud,1,2,3,4 Jess M. Schultz,5 Michael R. Lasarev,6 Philip J. S. Stork,4,7 and Kent L. Thornburg1,2,4
Departments of 1Physiology and Pharmacology, 2Medicine (Cardiology), and 5Surgery, 3Portland Veterans Affairs Medical Center, 6Center for Research on Occupational and Environmental Toxicology, 7The Vollum Institute, and 4Heart Research Center, Oregon Health and Science University, Portland, Oregon 97239

Submitted 30 April 2003 ; accepted in final form 21 August 2003


Growth of the fetal heart involves cardiomyocyte enlargement, division, and maturation. Insulin -like growth factor-1 (IGF-1) is implicated in many aspects of growth and is likely to be important in developmental heart growth. IGF-1 stimulates the IGF-1 receptor (IGF1R) and downstream signaling pathways, including extracellular signal-regulated kinase (ERK) and phosphoinositol-3 kinase (PI3K). We hypothesized that IGF-1 stimulates cardiomyocyte proliferation and enlargement through stimulation of the ERK cascade and stimulates cardiomyocyte differentiation through the PI3K cascade. In vivo administration of Long R3 IGF-1 (LR3 IGF-1) did not stimulate cardiomyocyte hypertrophy but led to a decreased percentage of cells that were binucleated in vivo. In culture, LR3 IGF-1 increased myocyte bromodeoxyuridine (BrdU) uptake by three- to five-fold. The blockade of either ERK or PI3K signaling (by UO-126 or LY-294002, respectively) completely abolished BrdU uptake stimulated by LR3 IGF-1. LR3 IGF-1 did not increase footprint area, but as expected, phenylephrine stimulated an increase in binucleated cardiomyocyte size. We conclude that 1) IGF-1 through IGF1R stimulates cardiomyocyte division in vivo; hyperplastic growth is the most likely explanation of IGF-1 stimulated heart growth in vivo; 2) IGF-1 through IGF1R does not stimulate binucleation in vitro or in vivo; 3) IGF-1 through IGF1R does not stimulate hypertrophy either in vivo or in vitro; and 4) IGF-1 through IGF1R requires both ERK and PI3K signaling for proliferation of near-term fetal sheep cardiomyocytes in vitro.

hyperplasia; hypertrophy; UO-126; LY-294002

[KGBnine]

good article flex...would this developmental heart growth occur mostly in sub-q injections, or with IM injections also? and is this good or bad? (Einstein, anyone?)

[einstein1905]

good article flex...would this developmental heart growth occur mostly in sub-q injections, or with IM injections also? and is this good or bad? (Einstein, anyone?)

Keep in mind this is the fetal heart. During development, there are many genes that are expressed that aren't expressed when mature and vice versa. I doubt that the concentration of IGF receptors on cardiac myocytes are nearly what they are during fetal development.
Organ growth is a slight possibility with GH or IGF-1, but the doses that one would normally need to see that would be very high for long durations.
Nice find on the article though.

[northendninja]

i dont have nearly enough schooling yet to translate that into an understandable form , so thanks for the translation einstein! good read.