title: Effects of a polyclonal antiserum to rat growth hormone on circulating insulin-like growth factor (IGF)-I and IGF-binding protein concentrations and the growth of muscle and bone.
abstract: A polyclonal antiserum to rat GH (anti-rGH) injected into rats for 3 or 8 weeks markedly reduced the weight, total protein and RNA content of muscles of the hind limb. These effects were prevented when bovine GH (bGH) was administered simultaneously. In a second experiment, the effects of 8 weeks of treatment with anti-rGH on the growth of the whole body, muscle and bone were investigated. Body weights of rats were decreased by 58% by treatment with anti-rGH; muscle weights were reduced by slightly more than the decrease in body weight (by 64%, 65% and 61% respectively for plantaris, soleus and gastrocnemius). The weight of the tibia was decreased by 54%, its length was decreased by 23%, cortical width and overall width were reduced by 26% and 18% respectively, suggesting a possible role for GH in osteoclastic activity. Serum total insulin-like growth factor-I (IGF-I) concentrations were decreased by 80-90% in both experiments by anti-rGH; these changes were prevented in the first experiment by concurrent treatment with anti-rGH and bGH. The serum IGF-binding protein-3 (IGFBP-3) concentration was also decreased by anti-rGH in experiment 1 (by 86%); the response of the 28-32 kDa IGFBPs was smaller (-35%), and was restored to control values by simultaneous injection of bGH. Western immunoblotting using an antiserum to IGFBP-2 showed that there was a marked decrease from neonatal to adult stages which was independent of anti-rGH treatment. This clearly demonstrated a dissociation of the reciprocal relationship supposed to exist between IGFBPs-2 and -3. The 24 kDa IGFBP-4 was unaffected by anti-rGH but replacement therapy with bGH doubled its concentration. Although the effects on body and muscle weight were prevented when rats were given anti-rGH and bGH simultaneously, the possibility of mediation by other hormones cannot be precluded.
authors.affiliation: Rowett Research Institute, Bucksburn, Aberdeen, UK.
authors.forename: R M
authors.initials: RM
authors.lastname: Palmer
authors.forename: N
authors.initials: N
authors.lastname: Loveridge
authors.forename: B M
authors.initials: BM
authors.lastname: Thomson
authors.forename: S C
authors.initials: SC
authors.lastname: Mackie
authors.forename: E
authors.initials: E
authors.lastname: Tonner
authors.forename: D J
authors.initials: DJ
authors.lastname: Flint
mesh_terms: D000818:Animals; D001835:Body Weight / Q000502:physiology; D001846:Bone Development / Q000502:physiology*; D002352:Carrier Proteins / Q000097:blood*; D005260:Female; D013006:Growth Hormone / Q000276:immunology / Q000494:pharmacology / Q000502:physiology*; D006131:Growth Inhibitors / Q000097:blood*; D007106:Immune Sera; D018969:Insulin-Like Growth Factor Binding Proteins; D007334:Insulin-Like Growth Factor I / Q000378:metabolism*; D024510:Muscle Development; D051381:Rats; D017208:Rats, Wistar
chemical_list: D002352:Carrier Proteins; D006131:Growth Inhibitors; D007106:Immune Sera; D018969:Insulin-Like Growth Factor Binding Proteins; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone