| Autor: |
Talmage RV; Department of Orthopaedics, UNC School of Medicine, Chapel Hill, NC, USA. RVTalmage@AOL.com, Mobley HT |
| Jazyk: |
angličtina |
| Zdroj: |
General and comparative endocrinology [Gen Comp Endocrinol] 2008 Mar 01; Vol. 156 (1), pp. 1-8. Date of Electronic Publication: 2007 Nov 12. |
| DOI: |
10.1016/j.ygcen.2007.11.003 |
| Abstrakt: |
The purpose of this report is to adjust our interpretation of the actions of parathyroid hormone (PTH) to include its action on the bone mineral-noncollagenous protein interactions at all bone surfaces. The three primary areas that respond to PTH are: (1) all bone surface areas in contact with the extracellular fluid (ECF), (2) the kidney, and indirectly the intestinal tract, and (3) the bone remodeling sequence. The primary rapid action of the hormone is to set and maintain the free calcium concentration of the ECF. This it does by raising the equilibrium level at bone mineral surfaces. It affects the noncollagenous protein bone mineral process to raise the free calcium level in the ECF from the base level of 3.5mg/100ml to the physiological level of 5.0mg/100ml. Maintaining the higher level requires continuous secretion of parathyroid hormone. The action of PTH at bone surfaces tends to be catabolic in nature in regard to bone loss. The hormone also acts on the kidney to raise the threshold for calcium reabsorption and by stimulation of renal hydroxylation of vitamin D to increase intestinal absorption of calcium. Its action here is to supply the ECF with calcium derived from food intake. This is the extent of PTH action on renal processes. PTH acts on all three steps in the bone remodeling process. While its total function here is not clear, the result is a net increase in the synthesis of collagen. The report concludes by comparing the actions of PTH as proposed here to the functions of PTH that have been proposed in the past. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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