Human growth hormone: Difference between revisions
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'''Glycosylation'''<br/> | '''Glycosylation'''<br/> | ||
Glycosylation helps distinguish between different variants and isoforms as it works as an ID cards for proteins. These carbohydrates are specific to each forms and are recognized by the associated hgH receptors. Though still being a relatively unknown mechanism in hgH, studies have shown that one isoform in particular, a 22kDa variant was identified and discovered due to the specific carbohydrates linked to its polypeptide chain. | Glycosylation helps distinguish between different variants and isoforms as it works as an ID cards for proteins. These carbohydrates are specific to each forms and are recognized by the associated hgH receptors. Though still being a relatively unknown mechanism in hgH, studies have shown that one isoform in particular, a 22kDa variant was identified and discovered due to the specific carbohydrates linked to its polypeptide chain (M.Kirstein 1992). | ||
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'''Somatostatin'''<br/> | '''Somatostatin'''<br/> | ||
The body’s primary mechanism | The body’s primary mechanism for regulating hGH is to release somatostatin, also known as growth hormone inhibitory hormone (GHIH). Somatostatin is produced in the hypothalamus and released by the anterior pituitary gland, pancreas, and GI tract (Somatostatin, 2011). This hormone works together with growth hormone releasing hormone (GHRH) to properly regulate the secretion of hGH from the pituitary gland. Somatostatin levels are directly affected by levels of circulating hGH. Specifically, levels of somatostatin are high when hGH concentrations are high, and low when hGH is low. | ||
There are two forms of somatostatin found in the body. One form, known as SS-14, is 14 amino acids long and found primarily in the nervous system and pancreas. The other has an amino acid chain length of 28 and is called SS-28. This form is found predominantly in the GI tract. SS-28 is a much stronger inhibitor of hGH then SS-14 (Bowen, 2002). Most of the body’s receptors | There are two forms of somatostatin found in the body. One form, known as SS-14, is 14 amino acids long and found primarily in the nervous system and pancreas. The other form has an amino acid chain length of 28 and is called SS-28. This form is found predominantly in the GI tract. SS-28 is a much stronger inhibitor of hGH then SS-14 (Bowen, 2002). Most of the body’s receptors do not differentiate between the two forms of somatostatin. All receptors are G protein-coupled receptors and inhibit adenyl cyclase, which, in turn, affects a number of hormones and second messengers (Bowen, 2002). | ||
'''Glucocorticoids'''<br/> | '''Glucocorticoids'''<br/> | ||
Glucocorticoids are a type of steroid hormones that regulate hGH levels two different ways. Studies have shown that glucocorticoids are able to suppress the release of GHRH as well as reduce GHRH receptor responsiveness (Miller et al., 1997)<ref>PMID:9165036</ref>. Due to the suppression of GHRH, the levels of hGH in the body eventually subside. There is also data to suggest that glucocorticoids work with somatostatin release in the hypothalamus (Lima et al., 1993)<ref>PMID:8094392</ref>. | Glucocorticoids are a type of steroid hormones that regulate hGH levels in two different ways. Studies have shown that glucocorticoids are able to suppress the release of GHRH as well as reduce GHRH receptor responsiveness (Miller et al., 1997)<ref>PMID:9165036</ref>. Due to the suppression of GHRH, the levels of hGH in the body eventually subside. There is also data to suggest that glucocorticoids work with somatostatin release in the hypothalamus (Lima et al., 1993)<ref>PMID:8094392</ref>. | ||
Besides interactions with GHRH and somatostatin, glucocorticoids can affect adrenergic receptors (both [[Adrenergic receptor|alpha 2-adrenergic and beta-adrenergic receptors]], which are stimulated by catecholamines in the sympathetic nervous system. When stimulated, the alpha receptors have shown to stimulate hGH release, whereas stimulation of beta receptors can inhibit hGH release (Blackard, 1968). | Besides interactions with GHRH and somatostatin, glucocorticoids can affect adrenergic receptors (both [[Adrenergic receptor|alpha 2-adrenergic and beta-adrenergic receptors]], which are stimulated by catecholamines in the sympathetic nervous system. When stimulated, the alpha receptors have shown to stimulate hGH release, whereas stimulation of beta receptors can inhibit hGH release (Blackard, 1968). | ||
'''Hyperglycemia and Insulin'''<br/> | '''Hyperglycemia and Insulin'''<br/> | ||
Periods of high sugar levels in the body are generally accompanied with higher insulin levels. In this state, insulin and related hormones like Insulin-like Growth Factor (IGF-1) have been shown to decrease binding affinity between hGH and its receptors (Shaonin et al., 1997). With lower levels of insulin and IGF-1, hGH secretion and levels can quickly and continuously rise. Although insulin and IGF-1 don't directly act on hGH receptors, they can affect the signaling cascade pathway that hGH uses (Yakar et al., 2004)<ref>PMID:14702113</ref>. JAK2 is one of the proteins found in this signaling pathway and it has been known to be affected during hGH/insulin feedback and regulation loops (Shaonin et al., 1997). | |||
==Associated Diseases and Treatments== | ==Associated Diseases and Treatments== |