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Journal Article

Effects of administration of somatostatin‐14 and immunoneutralization of somatostatin on endocrine and growth responses in rainbow trout

B. C. Peterson; P. R. Simpson; K. D. Cain; R. H. Hardy; G. T. Schelling; T. L. Ott
Journal of Fish Biology · Vol. 63, Issue 2 · pp. 506-522 · 2003

Abstract

Injection of somatostatin‐14 (SS‐14) at 5 ng g −1 body mass (BM) into rainbow trout Oncorhynchus mykiss decreased ( P r 2 = 0·54) levels of growth hormone (GH) (1·5 ± 0·9 ng ml −1 v. 6·6 ± 0·6 ng ml −1 ) over time when compared to controls. Somatostatin‐14 at 50 ng g −1 BM also decreased ( P = 0·064, q uadratic; r 2 = 0·30) levels of GH (3·6 ± 2·1 ng ml −1 v. 6·6 ± 0·6 ng ml −1 ) over time compared to controls. In a second study, passive immunization against SS‐14 (1 : 25 dose) increased ( P = 0·10, cubic, r 2 = 0·12) levels of GH (11·0 ± 4·8 ng ml −1 v. 5·2 ± 1·4 ng ml −1 ) over time. Passively immunizing against SS‐14 (1 : 50 dose) increased ( P r 2 = 0·10) levels of GH (8·2 ± 2·3 ng ml −1 v. 5·2 ± 1·4 ng ml −1 ) over time compared to controls. Overall, in the active immunization study there was no difference ( P > 0·10) in specific growth rate ( G ) or feed conversion ratio ( FCR ) between the three treatment groups during the 9 weeks of the study. Only four of the fish immunized against SS‐14, however, developed antibody titres against SS. Compared to controls, these fish exhibited a G of 0·89 ± 0·09 v. 0·56 ± 0·09% per 3 weeks and FCR of 0·80 ± 0·04 v. 1·20 ± 0·05 g g −1 . In SS‐14 immunized fish, levels of GH decreased ( P P G and FCR is dependent upon generation of antibody titres.

Bibliographic Information

JournalJournal of Fish Biology
PublisherWiley
Publication Date2003-08-01
Publication Year2003
Volume63
Issue2
Pages506-522
Document TypeJournal Article
Print ISSN0022-1112
eISSN1095-8649
DOI10.1046/j.1095-8649.2003.00177.x
SubjectGeneral Aquaculture, Fisheries & Fish Science

Access Information

NARA Access Coverage1997-01-01~Current
Journal Homepagehttps://onlinelibrary.wiley.com/loi/10958649
Publisher PageOpen Publisher Page
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