theory for ultimate cutting cycle with igf and t3

  1. theory for ultimate cutting cycle with igf and t3

    If what i read in the stickies is correct and that igf actually inhibits the loss of glyocogen from the muscle and forces the body to use fat and blood sugar as its primary energy source. Then by supplementing T3 with igf would yeild an expenential fat loss, and the loss of muslce mass would be considerably less if nut completly negated by the effects of IFG. This is just a theory of course. what do u guys think

  2. Thyroid Hormone Action

    Thyroid hormone stimulates bone growth by increasing the action of insulin-like growth factor-I

    The background of the study. Thyroid hormone is essential for normal bone growth in children, and it stimulates the turnover of bone in adults. In children and adults with hypothyroidism, the production of growth hormone and insulin-like growth factor (IGF)-I, which are needed for normal growth, are decreased, but the decreases may not be sufficient to account for the growth retardation in the children. Bone cells contain receptors for thyroid hormone; therefore thyroid hormone probably has direct effects on bone. This study evaluated the effects of triiodothyronine (T3) on the production of IGF-I, the receptors for IGF-I, and the growth-promoting actions of IGF-I in bone cells in vitro.

    How the study was done. Bone-forming cells (osteoblasts) were grown from pieces of bone obtained at the time of knee or hip joint replacement in six women and five men with osteoarthritis. The cultured cells were characterized as osteoblasts by several biochemical tests.

    The results of the study. Incubation of osteoblasts with T3 for 24 hours did not increase the cellular levels of IGF-I, but did increase the cellular levels of IGF-I receptors. T3 and IGF-I alone stimulated osteoblast proliferation, and the effect of IGF-I was amplified by exposing the cells to T3 before they were exposed to IGF-I.

    The conclusions of the study. In osteoblasts T3 increases IGF-I receptors and increases the ability of IGF-I to stimulate proliferation of the cells. These results help to explain why children with hypothyroidism grow poorly

    The original article. Pepene CE, Kasperk CH, Pfeilschifter J, Borcsok I, Gozariu L, Ziegler R, Seck T. Effects of triiodothyronine on the insulin-like growth factor system in primary human osteoblastic cells in vitro. Bone 2001;29:540-6.

  3. another

    Thyroid growth and function are increased in mice in which the growth-promoting substance, insulin-like growth factor-I, and its receptor are expressed in thyroid tissue

    The background of the study. Insulin-like growth factor-I (IGF-I), acting via its receptor on cells, stimulates the growth of many tissues. In this study the gene for IGF-I, the gene for the IGF-I receptor, and both genes, were introduced into thyroid tissue of mice to determine if thyroid growth and function were affected.

    How the study was done. Transgenic mice were produced by injecting portions of the human IGF-I gene or the IGF-I receptor gene into fertilized mouse eggs. Mice carrying each gene were bred together to obtain mice bearing both genes. Expression of the two genes was verified by detection of the gene products in thyroid tissue of these mice, but not in thyroid tissue from normal mice.

    The results of the study. The body weight and behavior of the transgenic mice were similar to that of normal mice. The weight of the thyroid glands and the thyroid function were higher in the mice with both transgenes.

    The conclusions of the study. In mice, insertion of the genes for IGF-I and its receptor in thyroid tissue results in increased thyroid growth and function. Increases in these two substances in thyroid tissue could play a role in the causation of goiter in humans.

    The original article. Clement S, Refetoff S, Robaye B, Dumont JE, Schurmans S. Low TSH requirement and goiter in transgenic mice overexpressing IGF-I and IGF-I receptor in the thyroid gland. Endocrinology 2001;142:5131-9.

  4. Thyroid hormones are important for growth and development of many tissues. Altered thyroid
    hormone status causes testicular abnormalities. For instance, juvenile hypothyroidism

    transient hypothyroidism induces macroorchidism, increases testicular cell number (Sertoli,
    Leydig, and germ cells) and daily sperm production. Triiodothyronine (T3) receptors have been
    identified in sperm, developing germ cells, Sertoli, Leydig, and peritubular cells. T3 stimulates Sertoli
    cell lactate secretion as well as mRNA expression of inhibin-
    a, androgen receptor, IGF-I, and

    IGFBP-4. It also inhibits Sertoli cell mRNA expression of M
    ullerian inhibiting substance (MIS),

    aromatase, estradiol receptor, and androgen binding protein (ABP) and ABP secretion. T3 directly
    increases Leydig cell LH receptor numbers and mRNA levels of steroidogenic enzymes and steroidogenic
    acute regulatory protein. It stimulates basal and LH-induced secretion of progesterone, testosterone,
    and estradiol by Leydig cells. Steroidogenic factor-1 acts as a mediator for T3-induced
    Leydig cell steroidogenesis. Although the role of T3 on sperm, germ, and peritubular cells has not
    yet been completely studied, it is clear that T3 directly regulates Sertoli and Leydig cell functions.
    Further studies are required to elucidate the direct effect of T3 on sperm, germ, and peritubular

  5. Anyone else got an opinion, sorry about all the post but this has been the only board that has a designated forum for IGF. Someone was trying to tell me that T3 would increase IGF-BP, according to what I've read this is a small case but the overall effect is exponential because T3 activates more IGF receptors and in vivo the effects of IGF are amplified by T3 or pre-use of. Anyway i'm new to this board so I thought I'd contribute.
    Thanks guys

  6. cripes! I am gonna have to print that out and use it for reading in the "throne" room. I will have to summon all my powers of concentration

  7. Cliff notes please......

  8. Good post game, i cant wait for more people to chime in on this.

  9. So what would be a good dosage of T3 to go with 33,cg per day of Igf R3 ?

  10. I have a more complete profile on the synergistic effects of T3 and IGF-I, its pretty awesome if you like to check it out in the new T3 I made at IBE in addition to these old post.


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