IGF-2 is a member of the insulin family of polypeptide growth factors that is involved in development and growth. It is an imprinted gene and is expressed only from the paternally inherited allele. It is a candidate gene for eating disorders. There is a read-through, INS-IGF2, which aligns to this gene at the 3’ region and to the upstream INS gene at the 5’ region. Two alternatively spliced transcript variants encoding the same protein have been found for this gene.
In "layman’s" words, IGF-2 Long R3 exhibits a neuron protective effect similar to IGF-1 Long R3 and has many of the same properties that IGF-1 has. What does this mean for today’s researcher well when IGF-2 LR3 combined with IGF-1 LR3 it intensifies and creates a symbiotic relationship with IGF-1 creating a beneficial response to the two. IGF-2 also increases something called Steroidogenesis, which is the bodies’ affinity to produce its own natural hormones. Due to this affinity it also exhibits stronger fat burning properties than IGF-1 and the combination of the two seems to be profound. In terms of muscle mass IGF-2 Long R3 causes a greater transfixion assay in mouse C2C12 myoblasts. What this essentially may transpire to is that there is some sort of inhibition of myostatin derived from the combination of the two. Of course this is conjecture as there has been incredibly little research done on this peptide and it is really only found in the body during gestation so caution should be exhibited when performing research on this peptide. Was found in some researches that a dosage of around 10 to 15mcgs will prove effective to start when combined with an equal dose of IGF-1 Long R3 and increased from there on in once the rat’s body react to it. The results from this research were found to be quite remarkable.
In rodents IGF-2 Long R3 is available to all the IGF receptors not just one set of receptors as IGF-1 Long R3 does, now what are the benefit of giving CJC-1295 and GHRP-6 to a rat? Well, CJC and GHRP are a potent inducer of GH in the pituitary gland. IGF is a cell signaler and potent growth activator, now the more GH the rat has the more cell repair and growth activation that can take place within a rodent. The hypertrophy that occurs is far greater than that of just each one alone and greater than that which occurs with just IGF-1 alone. Hence the benefit.
"Below is an article from an endo journal - J Guan, CE Williams, SJ Skinner, EC Mallard and PD Gluckman Research Centre for Developmental Medicine and Biology, University of Auckland, New Zealand."
"Insulin-like growth factor (IGF)-1, IGF binding protein (IGFBP)-2, and IGFBP-3 are expressed in the rat brain in regions of neuronal loss by 3 days after hypoxic- ischemic (HI) brain injury and IGF-2 somewhat later. Central administration of rh-IGF-1 after HI injury reduces neuronal loss in vivo. To clarify the mode of action of IGF-1 and the potential role of IGFBPs, the effects of IGF-1, IGF-2, des(1-3)-N-IGF-1 (des-IGF-1), an analogue of IGF-1 with low affinity for IGFBPs, and IGF- 1 combined with IGF-2 were compared 2 h after administration into the lateral cerebral ventricle after an HI injury. Unilateral HI was induced in adult rats by right carotid artery ligation followed by 10- min exposure to 6%O2. The extent of neuronal loss was determined in the cortex, striatum, hippocampus, dentate gyrus, and thalamus 5 days later. Central administration of 20 micrograms IGF-1 (n = 17) reduced neuronal loss in all regions (P < 0.01). Neither 20 micrograms IGF-2 (n = 17), 2 micrograms des-IGF-1 (n = 10), nor 20 micrograms des-IGF-1 (n = 17) reduced neuronal loss. There was a trend towards a reduction in neuronal loss after 150 micrograms des-IGF-1 (n = 20). IGF-2 alone increased neuronal loss in the hippocampus and dentate gyrus compared with the same regions in vehicle-treated animals (P < 0.05). Coadministration of 30 micrograms IGF-2 blocked the neuroprotective effects of 20 micrograms IGF-1 (n = 18, P < 0.05) and reduced the accumulation of [3H]IGF-1 in the injured hemisphere (n = 4) (P < 0.05). These observations suggest a role for IGFBPs in targeting the neuroprotective actions of IGF-1. IGF-2 may antagonize the protective effect of IGF-1 by displacing it from IGFBPs."
In "layman’s" words, IGF-2 Long R3 exhibits a neuron protective effect similar to IGF-1 Long R3 and has many of the same properties that IGF-1 has. What does this mean for today’s researcher well when IGF-2 LR3 combined with IGF-1 LR3 it intensifies and creates a symbiotic relationship with IGF-1 creating a beneficial response to the two. IGF-2 also increases something called Steroidogenesis, which is the bodies’ affinity to produce its own natural hormones. Due to this affinity it also exhibits stronger fat burning properties than IGF-1 and the combination of the two seems to be profound. In terms of muscle mass IGF-2 Long R3 causes a greater transfixion assay in mouse C2C12 myoblasts. What this essentially may transpire to is that there is some sort of inhibition of myostatin derived from the combination of the two. Of course this is conjecture as there has been incredibly little research done on this peptide and it is really only found in the body during gestation so caution should be exhibited when performing research on this peptide. Was found in some researches that a dosage of around 10 to 15mcgs will prove effective to start when combined with an equal dose of IGF-1 Long R3 and increased from there on in once the rat’s body react to it. The results from this research were found to be quite remarkable.
In rodents IGF-2 Long R3 is available to all the IGF receptors not just one set of receptors as IGF-1 Long R3 does, now what are the benefit of giving CJC-1295 and GHRP-6 to a rat? Well, CJC and GHRP are a potent inducer of GH in the pituitary gland. IGF is a cell signaler and potent growth activator, now the more GH the rat has the more cell repair and growth activation that can take place within a rodent. The hypertrophy that occurs is far greater than that of just each one alone and greater than that which occurs with just IGF-1 alone. Hence the benefit.
"Below is an article from an endo journal - J Guan, CE Williams, SJ Skinner, EC Mallard and PD Gluckman Research Centre for Developmental Medicine and Biology, University of Auckland, New Zealand."
"Insulin-like growth factor (IGF)-1, IGF binding protein (IGFBP)-2, and IGFBP-3 are expressed in the rat brain in regions of neuronal loss by 3 days after hypoxic- ischemic (HI) brain injury and IGF-2 somewhat later. Central administration of rh-IGF-1 after HI injury reduces neuronal loss in vivo. To clarify the mode of action of IGF-1 and the potential role of IGFBPs, the effects of IGF-1, IGF-2, des(1-3)-N-IGF-1 (des-IGF-1), an analogue of IGF-1 with low affinity for IGFBPs, and IGF- 1 combined with IGF-2 were compared 2 h after administration into the lateral cerebral ventricle after an HI injury. Unilateral HI was induced in adult rats by right carotid artery ligation followed by 10- min exposure to 6%O2. The extent of neuronal loss was determined in the cortex, striatum, hippocampus, dentate gyrus, and thalamus 5 days later. Central administration of 20 micrograms IGF-1 (n = 17) reduced neuronal loss in all regions (P < 0.01). Neither 20 micrograms IGF-2 (n = 17), 2 micrograms des-IGF-1 (n = 10), nor 20 micrograms des-IGF-1 (n = 17) reduced neuronal loss. There was a trend towards a reduction in neuronal loss after 150 micrograms des-IGF-1 (n = 20). IGF-2 alone increased neuronal loss in the hippocampus and dentate gyrus compared with the same regions in vehicle-treated animals (P < 0.05). Coadministration of 30 micrograms IGF-2 blocked the neuroprotective effects of 20 micrograms IGF-1 (n = 18, P < 0.05) and reduced the accumulation of [3H]IGF-1 in the injured hemisphere (n = 4) (P < 0.05). These observations suggest a role for IGFBPs in targeting the neuroprotective actions of IGF-1. IGF-2 may antagonize the protective effect of IGF-1 by displacing it from IGFBPs."
