Growth hormone’s release is pulsatile. There are spikes of GH release with an overall low concentration in the body. Therefore, its measurement is meaningless. GH targets fat and liver cells to produce IGF-1. Insulin induced hypoglycemia stimulates GH release and hyperglycemia inhibits GH release.
GH action occurs when it binds to its membrane receptor. Membrane receptor binding activates tyrosine kinase JAK-2. JAK-2 phosphorylates proteins involved in signaling pathways. Phosphorylation of such proteins leads to difference effects in different specific cell types.
A second, indirect, action of GH is the anabolic buildup of the body. The growth promoting effects of GH are mediated through IGF-1 and IGF-2. IGF is produced by the liver in response to GH and promotes the growth of muscle, fat, and bone.
|
Direct Effects of GH |
Indirect Effects of GH (via IGF-1) |
| Decreased insulin sensitivityIncreased lipolysis | Increased protein synthesisIncreased epiphyseal (bone) growth |
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Last updated October 2013
