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  1. #1
    Foxy Sphinx's Avatar
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    Understanding IGF-1/LR3

    Whelp, since theres incredibly so much misinformation out there, Ill hafta post this little article I wrote. This should give you the VERY BASICS of IGF-1... yes... this is the BASICS, its FAR FAR FAR FAR FAR FAR more complex than this.

    IGF-1: How it works
    IGF-1 stands for Insulin -like Growth Factor-one. Many types of cells in the human body express IGF-1 receptors, such as bone cells, muscle cells, brain cells, organ cells, skin cells, etc. IGF-1 is most commonly used by a cell in the stimulation of the process of cellular proliferation (the dividing of cells). Research ive seen shows that IGF-1 plays roles in increasing cellular hypertrophy too. IGF-1 has also been shown to inhibit cellular apoptosis (disintegration of cells into membrane-bound particles).

    IGF-1 and Insulin
    To settle some of the slin/IGF-1 confusion. IGF-I is related to insulin but it is not regulated at the secretory level such as insulin. It improves the conditions of diabetics by mechanisms of action I do not feel like explaining, but does NOT cause diabeties. IGF-1 also has a very insulin-like effect on the shuttling of nutrients into cells.

    IGF-1 and IGFBPs
    IGF-1 activity is directly controlled by high affinity IGF binding proteins (IGFBPs). They act as 'brake pedals' for the IGF-1 molecule. IGFBPs 'grab' the IGF-1 molecule and hold onto it, releasing it at a physiologically determined IGF-1 receptor. IGF-1 activity is indirectly controlled by protease activity (PA). IGF-1 is shown to increase proteolytic complexes and the divergent regulation of proteasomes in the degradation of cytosolic and nuclear proteins, which translates over to IGFBP's resulting in their degradation and fragmentation and in result to that, a lower IGFBP blood-plasma level, which means more IGF-1 free circulating. This is however all in correlation with free-circulating IGF-1.

    Another route of IGF-1 activity is of independant growth control by autocrine growth factor production. This is where the growth factor (in this case, IGF-1) is produced locally inside the cell. Autocrine IGF-1 activity is not regulated by IGFBPs, but rather by signal transductions in which an extracellular signal (typically a hormone or neurotransmitter) interacts with a receptor at the cell surface.

    LongR3
    LongR3 is the long chain version of IGF-1. LongR3 was developed for in vitro cell culture use, and still to this day is not accepted as viable for in vivo use (whatever). LongR3 has an extension that causes the compound to be too large to exit the vascular system and engage the IGF-1 receptor until, as with an ester, the extension degrades and releases the IGF-1. Without this extension, free exogenous-IGF-1 molecules would within minutes engage all the available receptors as there are not enough IGFPBs to do the job of holding them around for a duration that is truly usable for any effectiveness and therefore has insufficient duration of activity. At a glance, LongR3 has decreased IGFBP affinity, which translates to higher lvls of free-circulating IGF-1. Inhibiting IGFPBs is not necessarily the goal as it is both friend and foe -- yes it may render IGF-1 inert while it is complexed to it within the ternary complex described above, but it is this complex that allows the IGF-1 to remain in vivo for IGF-1 to be released eventually over time.

    Somatokine
    Somatokine is a rather new version of IGF-1. Somatokine was developed to replicate in vivo human IGF-1 where it is usually found in a ternary complex with IGFBP-3 and Acid Labile Subunit Protein (ALS). Somatokine is inferior relative to LongR3 for the purposes of exceeding genetics (elite bodybuilding). For this reason, I will not go any further into Somatokine. I will however say, that in the cases of using exogenous IGF-1 to help in fracture repair, burn recovery, and other clinical applications, Somatokine may very well be the superior choice.

    IGF-1 and Cancer
    One of my best friends dad works for the National Institute of Health doing cancer research. Ive spent countless hours in discussion with him about IGF-1 and cancer cells. He is hesistant to making any solid conclusions about exogenous IGF-1 administration and its effects/roles in cancer. However, I will explain the possible IGF-1 effects in cancer. When you hear of cancer, malignant cancer, people tend to think of uncontrolled cell division. Essentially though, these transformed cancerous cells are immortalized. Now, many changes are required for this to occur (i.e. increased telomerase, increased bcl-2, increased myc and decreased p53). In the development of cancer, we tend to think of carcingogens consisting of both initiators and promoters. For instance, some initiators are UV radiation and tobacco smoke, usually causing DNA damage or mutation, whereas promoters tend to stimulate cell division. A few examples are phorbol esters, hormones, and growth factors. Now, keep in mind both events, initiation and promotion, are required for the development of malignant cells. Normally a cell serves its purpose and then dies via apoptosis. However, malignant cells donít undergo apoptosis. They are, as I said before, immortal. The normal triggers to apoptosis are DNA damage, loss of cell-matrix contact, loss of cell to cell contact, and last but most certainly not least, lack of growth factors.

    When you introduce growth factors, you could be providing the catalyst for cancer formation, so to speak. Letís say, for instance, you get many sunburns during your lifetime. Now, letís say that one cell has its DNA damaged or altered. This, in and of itself, isnít too much of a concern as this is only one part of the equation, the iniation. The second part is the promoter (including growth factors). Well, letís imagine we introduce growth factors to the cell which has damaged or mutated DNA and it then begins to divide at a more and more rapid rate until it wonít stop. Now you have a tumor, which is now capable of even faster growth as well as being invasive (able to invade surrounding tissues) and metastatic (able to cause growth in completely unrelated and distant tissues) in regard to other tissues.

  2. #2
    Muscleguy is offline suspended
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    Good post!

  3. #3
    Foxy Sphinx's Avatar
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    Bump.

  4. #4
    asymmetrical1's Avatar
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    good read

  5. #5
    50%Natural's Avatar
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    I enjoyed also. While I have not picked up a college biology book in several years, I almost did understand all of the processes which were spoken of.

  6. #6
    CarbonCopy's Avatar
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    Quote Originally Posted by Foxy Sphinx
    Whelp, since theres incredibly so much misinformation out there, Ill hafta post this little article I wrote. This should give you the VERY BASICS of IGF-1... yes... this is the BASICS, its FAR FAR FAR FAR FAR FAR more complex than this.

    IGF-1: How it works
    IGF-1 stands for Insulin -like Growth Factor-one. Many types of cells in the human body express IGF-1 receptors, such as bone cells, muscle cells, brain cells, organ cells, skin cells, etc. IGF-1 is most commonly used by a cell in the stimulation of the process of cellular proliferation (the dividing of cells). Research ive seen shows that IGF-1 plays roles in increasing cellular hypertrophy too. IGF-1 has also been shown to inhibit cellular apoptosis (disintegration of cells into membrane-bound particles).

    IGF-1 and Insulin
    To settle some of the slin/IGF-1 confusion. IGF-I is related to insulin but it is not regulated at the secretory level such as insulin. It improves the conditions of diabetics by mechanisms of action I do not feel like explaining, but does NOT cause diabeties. IGF-1 also has a very insulin-like effect on the shuttling of nutrients into cells.

    IGF-1 and IGFBPs
    IGF-1 activity is directly controlled by high affinity IGF binding proteins (IGFBPs). They act as 'brake pedals' for the IGF-1 molecule. IGFBPs 'grab' the IGF-1 molecule and hold onto it, releasing it at a physiologically determined IGF-1 receptor. IGF-1 activity is indirectly controlled by protease activity (PA). IGF-1 is shown to increase proteolytic complexes and the divergent regulation of proteasomes in the degradation of cytosolic and nuclear proteins, which translates over to IGFBP's resulting in their degradation and fragmentation and in result to that, a lower IGFBP blood-plasma level, which means more IGF-1 free circulating. This is however all in correlation with free-circulating IGF-1.

    Another route of IGF-1 activity is of independant growth control by autocrine growth factor production. This is where the growth factor (in this case, IGF-1) is produced locally inside the cell. Autocrine IGF-1 activity is not regulated by IGFBPs, but rather by signal transductions in which an extracellular signal (typically a hormone or neurotransmitter) interacts with a receptor at the cell surface.

    LongR3
    LongR3 is the long chain version of IGF-1. LongR3 was developed for in vitro cell culture use, and still to this day is not accepted as viable for in vivo use (whatever). LongR3 has an extension that causes the compound to be too large to exit the vascular system and engage the IGF-1 receptor until, as with an ester, the extension degrades and releases the IGF-1. Without this extension, free exogenous-IGF-1 molecules would within minutes engage all the available receptors as there are not enough IGFPBs to do the job of holding them around for a duration that is truly usable for any effectiveness and therefore has insufficient duration of activity. At a glance, LongR3 has decreased IGFBP affinity, which translates to higher lvls of free-circulating IGF-1. Inhibiting IGFPBs is not necessarily the goal as it is both friend and foe -- yes it may render IGF-1 inert while it is complexed to it within the ternary complex described above, but it is this complex that allows the IGF-1 to remain in vivo for IGF-1 to be released eventually over time.

    Somatokine
    Somatokine is a rather new version of IGF-1. Somatokine was developed to replicate in vivo human IGF-1 where it is usually found in a ternary complex with IGFBP-3 and Acid Labile Subunit Protein (ALS). Somatokine is inferior relative to LongR3 for the purposes of exceeding genetics (elite bodybuilding). For this reason, I will not go any further into Somatokine. I will however say, that in the cases of using exogenous IGF-1 to help in fracture repair, burn recovery, and other clinical applications, Somatokine may very well be the superior choice.

    IGF-1 and Cancer
    One of my best friends dad works for the National Institute of Health doing cancer research. Ive spent countless hours in discussion with him about IGF-1 and cancer cells. He is hesistant to making any solid conclusions about exogenous IGF-1 administration and its effects/roles in cancer. However, I will explain the possible IGF-1 effects in cancer. When you hear of cancer, malignant cancer, people tend to think of uncontrolled cell division. Essentially though, these transformed cancerous cells are immortalized. Now, many changes are required for this to occur (i.e. increased telomerase, increased bcl-2, increased myc and decreased p53). In the development of cancer, we tend to think of carcingogens consisting of both initiators and promoters. For instance, some initiators are UV radiation and tobacco smoke, usually causing DNA damage or mutation, whereas promoters tend to stimulate cell division. A few examples are phorbol esters, hormones, and growth factors. Now, keep in mind both events, initiation and promotion, are required for the development of malignant cells. Normally a cell serves its purpose and then dies via apoptosis. However, malignant cells donít undergo apoptosis. They are, as I said before, immortal. The normal triggers to apoptosis are DNA damage, loss of cell-matrix contact, loss of cell to cell contact, and last but most certainly not least, lack of growth factors.

    When you introduce growth factors, you could be providing the catalyst for cancer formation, so to speak. Letís say, for instance, you get many sunburns during your lifetime. Now, letís say that one cell has its DNA damaged or altered. This, in and of itself, isnít too much of a concern as this is only one part of the equation, the iniation. The second part is the promoter (including growth factors). Well, letís imagine we introduce growth factors to the cell which has damaged or mutated DNA and it then begins to divide at a more and more rapid rate until it wonít stop. Now you have a tumor, which is now capable of even faster growth as well as being invasive (able to invade surrounding tissues) and metastatic (able to cause growth in completely unrelated and distant tissues) in regard to other tissues.
    You wrote this? Hmm.... Not to be a jerk, but I think you took a lot of this off the net. You need to at least give some credit to the author - http://www.t-mag.com/nation_articles/279cy.jsp

    Peace,
    CC

  7. #7
    Foxy Sphinx's Avatar
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    Quote Originally Posted by CarbonCopy
    You wrote this? Hmm.... Not to be a jerk, but I think you took a lot of this off the net. You need to at least give some credit to the author - http://www.t-mag.com/nation_articles/279cy.jsp

    Peace,
    CC

    Indeed.

    its more a compilation of everything on IGF-1, well, the basics at least.

    The cancer stuff mainly comes from that article, as cancer is not my specialty, nor something I have much interest in, but I know there has been tons of discussion about the possibilities of cancer from IGF1/GH, and that was a beautiful article outlining the possiblities, but not drawing a conclusion as I feel it would be inappropriate to draw a conclusion on this so early into its hypothesis, however in my cancer research, im very skeptical IGF-1/GH will play much a devestating role in its formation as the majority of tumor types arent even reponsive to hormones, infact, very few are.

  8. #8
    byu
    byu is offline Junior Member
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    Great Post. I'd be interested in some of your research...maybe a small bibliography

  9. #9
    50%Natural's Avatar
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    [QUOTE=Foxy Sphinx]Whelp, since theres incredibly so much misinformation out there, Ill hafta post this little article I wrote.

    Plagarism, nice.

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