Pretreatment with bovine growth hormone is as effective as treatment during metabolic stress to reduce catabolism in fasted lambs

Ogawa, Eishin, Breier, Bernhard H., Bauer, Michael K., Gallaher, Brian W., Grant, Pat A., Walton, Paul E., Owens, Julie A. and Gluckman, Peter D. 1996, Pretreatment with bovine growth hormone is as effective as treatment during metabolic stress to reduce catabolism in fasted lambs, Endocrinology, vol. 137, no. 4, pp. 1242-1248, doi: 10.1210/endo.137.4.8625895.

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Title Pretreatment with bovine growth hormone is as effective as treatment during metabolic stress to reduce catabolism in fasted lambs
Author(s) Ogawa, Eishin
Breier, Bernhard H.
Bauer, Michael K.
Gallaher, Brian W.
Grant, Pat A.
Walton, Paul E.
Owens, Julie A.ORCID iD for Owens, Julie A.
Gluckman, Peter D.
Journal name Endocrinology
Volume number 137
Issue number 4
Start page 1242
End page 1248
Total pages 7
Publisher Oxford University Press
Place of publication Oxford, Eng.
Publication date 1996-04-01
ISSN 0013-7227
Keyword(s) Animals
Blood Glucose
Body Weight
Fatty Acids, Nonesterified
Growth Hormone
Insulin-Like Growth Factor Binding Proteins
Recombinant Proteins
Stress, Physiological
Science & Technology
Life Sciences & Biomedicine
Endocrinology & Metabolism
Summary The effects of recombinant bovine GH (rbGH) treatment on the insulin-like growth factor (IGF) axis and protein metabolism during fasting induced metabolic stress were evaluated in young lambs. To explore whether rbGH pretreatment alone might offer a degree of protection against nutritional stress, we compared the effects of rbGH given only before or during the fasting-induced metabolic stress with that given over the whole period. The animals were fed ad libitum for 5 days (well fed phase) and then fasted for 70 h (fasted phase). The rbGH was administered during either the well fed and the fasted phase (G-G), only during the well fed phase (G-S), or only during the fasted phase (S-G), and the effects were compared with those of saline treatment throughout both phases (S-S; n = 7/group). The rate of net protein catabolism, analyzed on the final day of the study, was reduced (P < 0.001) to a similar degree in all rbGH-treated groups compared with that in the S-S group. rbGH pretreatment was as effective as rbGH administered during the catabolic phase. Plasma IGF-I was increased (P < 0.001) in the well fed phase by rbGH treatment and decreased in the fasted phase in all groups. The rbGH treatment during the fasted phase resulted in a smaller fall in plasma IGF-I levels than saline treatment (P < 0.05, G-G vs G-S and S-G vs. S-S), but no difference was observed in the specific binding of [125I]ovine GH to the hepatic membranes from animals of the different groups. There was a negative correlation between net protein catabolism and plasma IGF-I levels (r = -0.48; P < 0.01) and specific binding of [125I]ovine GH to hepatic membranes (r = -0.56; P < 0.001). Plasma IGF-II levels were decreased by rbGH treatment during the well fed phase, but the responses to treatment during the fasted phase were variable, suggesting that plasma IGF-II is regulated in a different manner than plasma IGF-I. The fasting-induced fall (P < 0.05) in plasma concentrations of IGF-binding protein (IGFBP)-3 was reduced with rbGH treatment, and plasma concentrations IGFBP-2 were altered in an inverse manner. This study suggests that fasting-induced GH resistance can be alleviated by rbGH treatment independent of whether treatment is commenced before or after the onset of catabolic stress. Our observation of prolonged anticatabolic action of prophylactic rbGH treatment supports the proposal that prophylactic use of GH may reduce the degree of catabolism associated with subsequent interventions and, thus, improve clinical outcome.
Language eng
DOI 10.1210/endo.137.4.8625895
Field of Research 07 Agricultural And Veterinary Sciences
11 Medical And Health Sciences
06 Biological Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©1996, The Endocrine Society
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Collection: Office of the Deputy Vice-Chancellor (Research)
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