Human growth hormone: Difference between revisions

<StructureSection load='3hhr' size='350' side='right' caption='Human growth hormone and the extracellular domain of its receptor (PDB entry [[3hhr]])' scene=''>

It was previously believed that after stimulating HGH secretion, membrane bound secretory vesicles containing the hormone dock at the cell plasma membrane. These vesicles were believed to become completely incorporated into the plasma membrane, and would later be retrieved via endocytosis, thus allowing for passive release of the HGH within the vesicles. However, this mechanism is not supported by experimental evidence, such as the appearance of empty and partially empty vesicles immediately after secretion.  Bhanu Jena’s laboratory has recently elucidated the molecular mechanism of cellular secretion. Their studies suggest that there is actually a new cellular structure called a porosome that is involved with the mechanism. Porosomes are “basket-like” structures residing at the plasma membrane that have a 100-150nm diameter opening to the extracellular environment (Figure 1). It involves several specific proteins like SNAP receptors or N-ethylmaleimide-sensitive factor. First, the GH is brought to the porosome using ATP and kinesins along microtubules. Then, rather than docking directly at the plasma membrane post secretion stimulation, membrane bound secretory vesicles fuse at the base of porosomes, which subsequently expel the vesicular contents (Figure 2). During stimulation, the opening dilates about 20-35% to aid in the expulsion of HGH. The porosome returns to the resting size once the process is complete (Anderson et al., 2004)<ref>PMID:15305891</ref>.  

Several hypothalamic hormones that control growth hormone release exist. The most major of these secretion stimuli is the growth hormone release factor (GHRH). Another factor has been discover : ghrelin is an acylated peptide directly responsible for a GH secretion from somatotropes. In contrast, the hormone known as somatostatin (SRIF) is known to suppress the release of GH by the somatotrope. These two hormones are the most well known, though it should be noted that there are multiple other control factors which both stimulate and suppress the release of HGH into the bloodstream (Anderson et al., 2004).

The general treatment for dwarfism is HgH injections. The sooner this treatment is started, the more effective it will be. These injections are applied anywhere from several times a week to once a day.

Injection of GH has been implicated in the development of Creutzfeldt-Jakob Disease. Several cases of such disease were proven related to subjects being recipient of pituitary derived hGH. This association has only been found in GH isolated from cadavers. Originally isolation of the protein from cadavers was the method of development for replacement therapies. Now recombinant methods of production are the main method for synthesis. There seems to be no association in recombinant DNA-produced GH and Creutzfeldt-Jakob disease2.  

Diseases can also result from levels of GH being too high. The effects of excess GH vary based on age. Gigantism is excess of GH during childhood and Acromegaly is excess of GH during adulthood (after bone growth has stopped). Symptoms of gigantism include delayed puberty, headache, increased sweating, and weakness3. Symptoms of acromegaly vary slightly and include carpal tunnel syndrome, weakness, joint pain, sleep apnea, and unintentional weight loss4.  

Acromegaly is most commonly treated with surgery. Removing the tumor in the pituitary gland can stop the excess release of growth hormone. Incomplete success of the surgery is often attributed to the size of the tumor: large tumors cannot always be completely removed, resulting in continued high levels of hormone release (Freda, 2002)<ref>PMID:9814451</ref>.  

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