Insulin receptor expression in primary and cultured osteoclast-like cells.
Skeletal growth is the net product of coordinated bone formation and resorption. Insulin is known to stimulate bone formation by actions on osteoblasts. It is not known whether insulin receptors are present on osteoclasts, or whether insulin regulates osteoclastic function. We present here immunocytochemical evidence of insulin receptor expression by mature mono- and multinucleated murine osteoclast-like cells generated in vitro, and in primary neonatal rat and mouse osteoclasts. Radiolabeled studies indicated that progressive enrichment of osteoclast-like cells in coculture was associated with increased insulin binding. When osteoclast-like cells generated in vitro were plated onto dentine slices, insulin dose-dependently inhibited pit formation by up to 80%, suggesting a role for insulin in osteoclast function. These data are consistent with an effect of insulin on bone resorption in addition to those previously recognized on bone formation, actions that together result in net bone growth.
Thomas
D M
DM
The University of Melbourne Department of Medicine, St. Vincent's Hospital, Victoria, Australia.
Udagawa
N
N
Hards
D K
DK
Quinn
J M
JM
Moseley
J M
JM
Findlay
D M
DM
Best
J D
JD
D000818:Animals; D001846:Bone Development / Q000187:drug effects; D002478:Cells, Cultured; D018920:Coculture Techniques; D004305:Dose-Response Relationship, Drug; D015726:Giant Cells / Q000187:drug effects / Q000378:metabolism; D007150:Immunohistochemistry; D007328:Insulin / Q000494:pharmacology*; D051379:Mice; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism; D010010:Osteoclasts / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D011972:Receptor, Insulin / Q000096:biosynthesis*
D007328:Insulin; D011972:Receptor, Insulin