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Parathyroid hormone and calcitonin modify inositol phospholipid metabolism in fetal rat limb bones
Author(s) -
Rappaport Mark S.,
Stern Paula H.
Publication year - 1986
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1002/jbmr.5650010202
Subject(s) - parathyroid hormone , inositol , endocrinology , phospholipid , phosphatidylinositol , medicine , calcitonin , bone remodeling , bone resorption , hormone , chemistry , inositol trisphosphate , biology , calcium , biochemistry , receptor , signal transduction , membrane
Inositol‐containing phospholipids are believed to be intimately involved in the first steps of cellular signalling by certain hormones and neurotransmitters. We examined whether parathyroid hormone (PTH) and calcitonin (CT), two hormones that affect bone physiology, would elicit changes in inositol‐phospholipid metabolism in cultured bone. [ 3 H]inositol readily entered into the tissue phospholipid pool in fetal rat limb bones, and incorporated into phosphatidylinositol (92.9%), phosphatidylinositol‐4‐P (4.5%), and phosphatidylinositol‐4,5‐P 2 (2.6%). PTH enhanced the incorporation of inositol into PtdIns in limb bones following 2‐ or 24‐h hormone treatments. The effect of PTH was dose dependent (EC 50 of 0.3–0.4 n M ) and occurred in a concentration range similar to that for hormone‐stimulated bone resorption. In contrast, 24‐h treatment with CT‐inhibited inositol incorporation, also in a dose‐dependent manner. Two‐hour CT treatment had variable effects on labeling. CT inhibited the stimulatory effect of PTH at both 2 and 24 h. The effects induced by PTH and CT were specific for PtdIns and were independent of the [ 3 H]inositol pool size. These results indicate that inositol‐phospholipid turnover can be modified during the action of these hormones on bone tissue. Although the time course of hormone‐stimulated inositol incorporation observed here is slower than that found in other tissues, the change in phosphatidylinositol metabolism could mediate delayed effects of PTH or CT. Alternatively, alterations induced by PTH and CT in bone cell membranes, cell populations, or in the mineralized matrix could conceivably result in secondary changes in phosphatidylinositol metabolism.