IG-FACTOR ONE ® Growth Factor
IG-FACTOR ONE ® R3 IGF-1 is a protein released by many tissues and affects virtually every cell in the body. The main synthesizing organs of IG-FACTOR ONE ® R3 IGF-1 is the liver, although a local level is also produced in the placenta, heart, lung, kidney, pancreas, spleen, small intestine, testicles. , ovaries, large intestine, brain, bone marrow, and pituitary gland. Production is stimulated by growth hormone (GH) and can be retarded by malnutrition, growth hormone insensitivity, lack of growth hormone receptors, or failure of the post-receptor signaling pathway ( second messenger) of GH including SHP2 and STAT5B. Approximately 98% of IG-FACTOR ONE ® R3 IGF-1 is always bound to one of 6 binding proteins (IGF-BP). IGFBP3, the most abundant protein, accounts for 80% of all IGF binding. IG-FACTOR ONE ® R3 IGF-1 binds to IGFBP-3 in a 1:1 molar ratio. This protein forms a 140,000 dalton ternary complex with IG-FACTOR ONE ® R3 IGF-1 and with an acid-labile subunit.
MECHANISM OF ACTION
Its main action is mediated by binding to its specific receptor, the insulin-like growth factor receptor 1, abbreviated as IGF1R, present in many types of tissues. On binding to IGF1R, a receptor tyrosine kinase, it initiates intracellular signaling; IG-FACTOR ONE ® R3 IGF-1 is one of the most powerful natural activators of PKB signal transduction, a stimulator of cell growth and destruction, and a potent inhibitor of programmed cell death.
IG-FACTOR ONE ® R3 IGF-1 is a major mediator of the effects of growth hormone (GH). Growth hormone is produced in the anterior pituitary gland and released into the bloodstream, and then stimulates the liver to produce IG-FACTOR ONE ® R3 IGF-1. IG-FACTOR ONE ® R3 IGF-1 then stimulates the growth of the body systemically, and has growth-promoting effects on almost all cells in the body, especially skeletal muscle, cartilage, bone, liver, nerves, skin, cells hematopoietic, and lung. In addition to its insulin-like effects, IG-FACTOR ONE ® R3 IGF-1 can also regulate cell development and growth, especially in nerve cells, as well as cellular DNA synthesis.
Therefore, deficiency of either growth hormone or IG-FACTOR ONE ® R3 IGF-1 would result in decreased height. GH deficient children are given recombinant GH to increase their size. Humans deficient in IG-FACTOR ONE ® R3 IGF-1, who are classified as having Laron syndrome, or Laron dwarfism, are treated with recombinant IG-FACTOR ONE ® R3 IGF-1. In cattle, circulating IG-FACTOR ONE ® R3 IGF-1 is related to reproductive performance.
RECEPTORS
IG-FACTOR ONE ® R3 IGF-1 binds to at least two cell membrane receptors: the IG-FACTOR ONE ® R3 IGF-1 receptor (IGF1R), and the insulin receptor. IG-FACTOR ONE ® R3 IGF-1 has a high affinity for the IG-FACTOR ONE ® R3 IGF-1 receptor, and a low affinity for the insulin receptor. These receptors are tyrosine kinases (meaning they signal by causing the addition of a phosphate molecule to certain tyrosines). IG-FACTOR ONE ® R3 IGF-1 activates the insulin receptor at approximately 0.1x the potency of insulin.
IG-FACTOR ONE ® R3 IGF-1 is produced throughout life. The highest levels occur during pubertal growth, the lowest in childhood and old age.
Other IGF-BPs (binding/transport proteins) are inhibitory. For example, both IGFBP-2 and IGFBP-5 bind to IG-FACTOR ONE ® R3 IGF-1 at an affinity greater than the affinity that IG-FACTOR ONE ® R3 IGF-1 binds to its receptor. Therefore, if the serum levels of these two IGF-BPs are increased, it would result in a decrease in the activity of IG-FACTOR ONE ® R3 IGF-1.
ANTI-AGE CONTRIBUTION
It is widely accepted that signaling through the insulin receptor/IG-FACTOR ONE ® R3 IGF-1 pathway is a significant contributor to the biological aging process in many organisms. This line of research gained prominence with the work of Cynthia Kenyon, who showed that mutations in the daf-2 gene could double the lifespan of an earthworm C. The daf-2 gene encodes the insulin/IG-FACTOR ONE ® R3 receptors worm IGF-1.
Insulin/IG-FACTOR ONE ® R3 IGF-1 signaling is conserved from worms to humans. According to studies subsequent to Kenyon's work, mutations that reduce insulin/IG-FACTOR ONE ® R3 IGF-1 signaling have been shown to slow the degenerative aging process and extend the life of a wide range of organisms, including Drosophila melanogaster, mice, [9] and possibly humans.
The reduction of IG-FACTOR ONE ® R3 IGF-1 signaling is also thought to contribute to the "anti-aging" effects of calorie restriction.
