Neurotrophic and Neuroregenerative Effects of GH/IGF1
Sep 4, GH and IGF-1 are associated with higher rates of cancer, both in humans in the receptor for GH, which interrupts the connection GH → IGF May 26, GH stimulates the synthesis of IGF-I in most tissues (Figure 1; d'Ercole et al., ; . In a muscle, the ratio of DNA/protein is fairly constant (Roy et al., ). [ PubMed]; Frick GP, Tai LR, Baumbach WR, Goodman HM. There is a big difference between Growth Hormone, and IGF The fact is, indeed, that Growth Hormone is broken down in the liver, and produces IGF-1 ( Insulin.
In embryonic cultures from cerebral cortex, it was demonstrated that GH stimulated neuronal precursor and glial cells [ 1819 ], increased neurogenesis, myelination, and synaptogenesis, [ 4 ]. In adults, GH administration regulates brain function, learning, memory, and neuroprotection [ 20 ]. Glial cells, including microglia, astrocytes, and oligodendrocyte lineage cells, are also strongly reactive to GH [ 1421 ].
Insulin-like growth factor 1
GH deficiency in mouse causes the reduction in oligodendroglial cells and the myelination process [ 22 ]. Astrocytes, which are the most abundant and well-studied type of glial cell in the adult brain [ 23 ], play a crucial role in the maintenance of brain health, protecting it by inflammation [ 24 ]. Oligodendrocytes are responsible for the myelin production in axons, and gives them trophic support, ensuring long-term integrity [ 26 ].
Loss of myelin is responsible of various neurological diseases, and contributes to neuropsychiatric disorders. Glial cells are involved in providing neurotrophic signals to neurons required for their survival, proliferation, and differentiation.
How To Use Growth Hormone Stacks
Furthermore, it is recognized that glial cells have some effects on certain physiological processes, such as breathing, and in assisting neurons to form synaptic connections amongst one another [ 27 ]. Astrocytes maintain the homeostatic environment of the CNS and play an important role in immune regulation, acting a source of chemokines, cytokines, and effector molecules [ 28 ]. Growth factors GFs typically act as signaling molecules between cells [ 29 ].
They perform an essential function in the route of signaling molecules between astrocytes and neurons [ 30 ]. GH-induced neuroprotection downregulating the apoptosis-promoting gene [ 31 ] protected the brain from hypoxic injury, attenuating caspase-3 expression [ 32 ]. These data indicated that exogenous GH therapy might exert a protective action against hypoxic-ischemic brain injury, and also promotes the proliferation of progenitor neural stem cells in the human fetal cortex [ 33 ].
Interestingly, GH affects most of the major brain neurotransmitters, including the monoamine such as serotonin and noradrenaline [ 34 ], the dopaminergic system [ 35 ], and stimulates dopaminergic activity [ 36 ]. IGF-1 has a more potent trophic effect, compared to GH, in the motor and sensory neurons, and on neuronal development and regeneration [ 3738394041 ]. A reduced IGF-1 signaling, due to mutation of IGF-1 and its receptor gene, caused microcephaly and mental impairment [ 4243 ].
IGF-1 promotes neurite outgrowth [ 17 ] and protects cells from apoptotic stimuli at mitochondrial level [ 44 ]. In denervated muscle tissue, IGF-1 stimulates muscle growth and regeneration, and prevents atrophy [ 464748 ].
Emerging promising results demonstrates that IGF-1 possesses a therapeutic effect on the brain by increasing hippocampal neurogenesis and memory accuracy in elderly individuals, and possibly, in neurodegenerative disorders [ 50 ].
An increasing amount of evidence is suggesting the potential usefulness of growth factors, such as IGF-I, as potential treatments for certain neurodegenerative diseases, including ALS and AD due to its neurotrophic effect [ 54 ]. Data about the effects of GH and IGF-1 administration in neurodegenerative diseases are still insufficient. This study aims to evaluate the effects of GH and IGF-1 therapy conducted in human and animal models on the peripheral and central nervous system, and future perspectives.
Between these search engines, Google Scholar provided a large amount of data, but is less selective.
Neurotrophic and Neuroregenerative Effects of GH/IGF1
A combination of the following keywords was used: IGFBP-1 is regulated by insulin. The highest rates of IGF-1 production occur during the pubertal growth spurt. The lowest levels occur in infancy and old age.
This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. September Learn how and when to remove this template message 3-d model of IGF-1 Protein intake increases IGF-1 levels in humans, independent of total calorie consumption.
Growth hormone is made in the anterior pituitary gland, is released into the blood stream, and then stimulates the liver to produce IGF IGF-1 then stimulates systemic body growth, and has growth-promoting effects on almost every cell in the body, especially skeletal musclecartilageboneliverkidneynerveskinhematopoieticand lung cells. Its primary action is mediated by binding to its specific receptor, IGF1R, which is present on the surface of many cell types in many tissues. Binding to the IGF1R initiates intracellular signaling.
IGF-1 is one of the most potent natural activators of the AKT signaling pathwaya stimulator of cell growth and proliferation, and a potent inhibitor of programmed cell death. IGF-1 activates the insulin receptor at approximately 0. A key pathway is regulated by phosphatidylinositol-3 kinase PI3K and its downstream partner, the mammalian target of rapamycin mTOR.
As the name "insulin-like growth factor 1" implies, IGF-1 is structurally related to insulin, and is even capable of binding the insulin receptor, albeit at lower affinity than insulin.
One such disorder, termed Laron dwarfism does not respond at all to growth hormone treatment due to a lack of GH receptors. As a result, these patients cannot be expected to respond to GH treatment.