Talk:Parathyroid hormone

This describes the discovery of PTH quite vividly. JFW | T@lk  23:49, 30 October 2006 (UTC)

Add info about clinical administration of PTH
I believe adding information about the clinical administration of PTH and the differing effects of sustained administration vs. pulsatile administration and their differing effects on bone density would be useful here. --Drewlew 05:07, 22 August 2007 (UTC)

Mg
magnesium can increase or decrease PTH, depending on the absolute value of the change... supposedly rhetoric 06:22, 22 October 2007 (UTC)

Low Mg is definitely associated with a decreased secretion of PTH Ianmc 20:12, 22 October 2007 (UTC)

The section of negative feedback needs to be changed. Right now it states osme information about G-protein coupling and really gets the whole mechanism wrong when it says that the cascade results in the trigger of vesicle fusion and exocytosis of the peptide. This is the exact opposite of what really happens. Instead:

The G-protein coupled calcium receptiors (CaR) sense extracellular calcium and may be found on the surface on a wide variety cells distributed in the brain, heart, skin, stomach, C cells, and other tissues. In the parathyroid gland, sensation of high concentrations of extracellular calcium result in activation of the Gq G-protein coupled cascade through the action of Phospholipase C. This hydrolyzes phosphatidylinositol 4,5-bisphosphae (PIP2) to liberate intracellular messengers IP3 and diacylglycerol (DAG). Ultimately, these two messengers result in a release of calcium from intracellular stores and a subsequent flux of extracellular calcium into the cytoplasmic space. The effect of this signaling of high extracellular calcium results in an intracellular calcium concentration which inhibits the secretion of preformed PTH from storage granules in the parathyroid gland. In contrast to the mechanism that most secretory cells use, calcium inhibits vesicle fusion and release of PTH. In the parathyroids, magnesium serves this role in stimulus-secretion coupling. Hypomagnesia may result in a paralysis of PTH secretion and lead to a form of hypoparathyroidism that is reversible.

Someone can make the links and source it. The source is Greenspan's Basic and Clinical Endocrinology 8th Ed. I don't have time nor do I know how. —Preceding unsigned comment added by 129.98.121.30 (talk) 17:08, 13 September 2010 (UTC)

I messed up the page a bit. Could someone who knows how remove the table. I deleted something in the formatting which left it. Please do not simply revert to saved. The information provided is more complete than BRS physiology. —Preceding unsigned comment added by 129.98.121.30 (talk) 17:14, 13 September 2010 (UTC)

Effects of PTH on Vitamin D
The article currently states that PTH "increas[es] the production of vitamin D AND upregulat[es] the enzyme responsible for 1-alpha hydroxylation of 25-hydroxy vitamin D..." [allcaps added for emphasis]

Is this referring to two effects of PTH on vitamin D, or one? If two, what is the process pf the first effect that increases the production of vitamin D. If one, then this should be clarified by stating, "increasing the production of vitamin D BY regulating..."

An answer to this question with a reference to a medical research or review article on the internet would be appreciated.

Leeirons (talk) 16:40, 11 December 2007 (UTC)

Diagnostic use
JFW &#124; T@lk  08:56, 24 December 2014 (UTC)

Assessment comment
Substituted at 02:16, 30 April 2016 (UTC)

Any discovered/verified function of the 50 C-terminal section?
It says that the PTH receptor (both of them I assume) only requires the first 34 amino acids, and Teriparatide consists of only this portion. Does anyone know of any research into whether the remaining 50 amino acids have some function we don't know about yet? I know there is research speculating on an advantageous function for the C-peptide portion of (pro)insulin, so I wonder if there is some undiscovered function for PTH as well. I found this reference on Google Books, which cites a few papers from around 2000, but can't find much else (I tried a search for "PTH C-Terminus") Jimw338 (talk) 12:29, 6 July 2016 (UTC)

Horribly written article
Another horribly written article by "writers", whom write only for themselves. This article is virtually useless to an average reader, and is more like reading a very, very poor textbook. It may have some value to chemists or medical students, but not to normal humans. It is poorly written, overly "wordy", and fails to describe the full function of this hormone, and more importantly, the lack of it (deficiency). This is another example of why I no longer contribute to WP. — Preceding unsigned comment added by 98.194.39.86 (talk) 14:29, 20 August 2016 (UTC)

Conflicting Information Regarding FGF23 Stimulation
In the section about "Regulation of PTH secretion" and under "Inhibitors", it states that FGF23 is produced in response to serum phosphate and indeed the source given agrees with this. However, in other Wikipedia articles (e.g. Fibroblast growth factor 23) and their accompanying sources, it is stated that FGF23 is produced in response to calcitriol. And in another source (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4815615/), it is stated that calcium directly regulates FGF23. So, which is it? Would be nice to have a definitive answer on this and fix all the pages that mention it.