title: Growth hormone and longitudinal bone growth in vivo: short-term effect of a growth hormone antiserum.
abstract: The control of longitudinal growth is poorly understood but GH is considered to be one of the major hormones regulating postnatal growth. However, there is dispute as to whether it has a direct or indirect action. To study the role of GH we used a polyclonal antiserum to rat GH and investigated changes in cell proliferation and enzyme activities associated with bone formation and resorption during longitudinal growth. IGF-I levels were measured by two independent RIAs, DNA synthesis by bromodeoxyuridine incorporation followed by immunocytochemistry and enzyme activities were quantified in situ by microdensitometry. After 1 day the percentage of chondrocytes undergoing DNA synthesis within the proliferative zone was reduced but no other parameters were affected. By day 4 the labelling index was the same as in pair-fed animals but the number of chondrocytes synthesising DNA was reduced as was the total width of the growth plate and that of the proliferative zone. Alkaline phosphatase (associated with mineralisation) was unchanged but glucose 6-phosphate dehydrogenase activity (associated with cell proliferation) was decreased. Osteoclastic tartrate-resistant acid phosphatase activity (associated with bone resorption) was also significantly reduced. Similar changes were apparent after 10 days. At no time was the circulating level of IGF-I decreased. These data suggest that, during longitudinal growth, GH affects the number of proliferating chondrocytes but not the percentage of cells undergoing DNA synthesis, indicating that its primary role may be on the commitment of prechondrocytes to a proliferative state. Furthermore, while GH does not seem to have any effect on skeletal mineralisation it may stimulate osteoclastic resorption of the primary spongiosa.
authors.affiliation: Division of Biochemical Sciences, Rowett Research Institute, Aberdeen, UK.
authors.forename: N
authors.initials: N
authors.lastname: Loveridge
authors.forename: C
authors.initials: C
authors.lastname: Farquharson
authors.forename: R
authors.initials: R
authors.lastname: Palmer
authors.forename: G E
authors.initials: GE
authors.lastname: Lobley
authors.forename: D J
authors.initials: DJ
authors.lastname: Flint
mesh_terms: D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D001846:Bone Development / Q000502:physiology*; D001862:Bone Resorption; D001842:Bone and Bones / Q000201:enzymology / Q000378:metabolism; D002455:Cell Division; D004247:DNA / Q000096:biosynthesis; D003720:Densitometry; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D013006:Growth Hormone / Q000276:immunology / Q000502:physiology*; D007106:Immune Sera / Q000494:pharmacology*; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D007527:Isoenzymes / Q000378:metabolism; D008297:Male; D011863:Radioimmunoassay; D051381:Rats; D011919:Rats, Inbred Strains; D000071681:Tartrate-Resistant Acid Phosphatase
chemical_list: D007106:Immune Sera; D007527:Isoenzymes; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D004247:DNA; D005954:Glucosephosphate Dehydrogenase; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase