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Interrelationship between parathyroid hormone and insulin: Effects on DNA synthesis in UMR‐106–01 cells
Author(s) -
Felsenfeld Arnold J.,
IidaKlein Akiko,
Hahn Theodore J.
Publication year - 1992
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.5650071112
Subject(s) - parathyroid hormone , medicine , endocrinology , thymidine , hormone , insulin , dna synthesis , in vitro , in vivo , secondary hyperparathyroidism , chemistry , biology , calcium , biochemistry , microbiology and biotechnology
UMR‐106–01 osteoblast‐like cells respond to high concentrations of parathyroid hormone (PTH) in vitro by decreasing thymidine incorporation, a marker of DNA synthesis and cell proliferation. This response is different from in vivo conditions, such as primary and secondary hyperparathyroidism, in which high PTH levels are associated with an increased number of osteoblasts. When the response of UMR‐106–01 cells to PTH is evaluated in vitro, however, these cells are exposed to only a single hormone. The present study was designed to evaluate the combined effects of two hormones, PTH and insulin, on the DNA synthesis of UMR‐106–01 cells. PTH is known to decrease and insulin to increase thymidine incorporation by UMR‐106–01 cells. To examine the interaction of these hormones, acute studies, defined as a 24 h exposure to hormone, and chronic studies, defined as a 7 day exposure to hormone, were performed. Both acute and chronic exposure to 10 −9 M PTH decreased thymidine incorporation by UMR‐106–01 cells, with suppression ranging from 27 to 81% ( P < 0.05). Both acute and chronic exposure to 10 −8 M insulin (INS) increased thymidine incorporation by UMR‐106–01 cells; this ranged from 26 to 58% ( P < 0.05). However, chronic exposure to 10 −9 M PTH followed by an acute exposure to 10 −8 M INS resulted in a 710% increase in thymidine incorporation ( P < 0.01). Reversing the sequence by chronically exposing UMR‐106–01 cells to 10 −8 M INS followed by acute exposure to 10 −9 M PTH resulted in a 53% decrease in thymidine incorporation ( P < 0.01). When 10 −9 M PTH and 10 −8 M INS were administered simultaneously, the increase in thymidine incorporation produced by acute and chronic administration ranged from 35 to 56% of nontreated control values ( P < 0.05). In conclusion, the timing of PTH and insulin administration may produce different responses in thymidine incorporation by UMR‐106–01 cells. Whether during hyperparathyroidism in vivo, pulsatile increases in insulin secretion are important for osteoblast proliferation remains to be determined.