|Simpson, Peggy - UNIV OF IDAHO, MOSCOW|
|Peterson, Brian - UNIV OF IDAHO, MOSCOW|
|Cain, Ken - UNIV OF IDAHO, MOSCOW|
|Hardy, Ron - UNIV OF IDAHO, HAGERMAN|
|Ott, Troy - UNIV OF IDAHO, MOSCOW|
Submitted to: Growth Hormone and IGF Research
Publication Type: Proceedings
Publication Acceptance Date: February 1, 2004
Publication Date: April 1, 2004
Citation: Simpson, P., Overturf, K.E., Peterson, B., Cain, K., Hardy, R., Ott, T. 2004. Physiological effects of recombinant bovine somatotropin (rbst) in rainbow trout (oncorhynchus mykiss). Growth Hormone and IGF Research. General and Comparative Endocrinology 135:324-333. Interpretive Summary: Treatment of many species with an exogenous source of somatotropin increases growth rates with increases in muscle mass. Several piscine species respond similarly to treatment with recombinant bovine somatotropin. Studies have shown increases in growth rates as great as 200% in as little as six weeks post-treatment. Since most teleosts exhibit indeterminate growth, as well as hyperplastic and hypertrophic skeletal muscle growth throughout their lives, it has been hypothesized that the growth regulatory system in these fish differs from mammals. It was recently shown that trout exhibit local production of somatotropin in tissues important in functions other than overall growth regulation. It is therefore hypothesized that treatment with recombinant bovine somatotropin (rbST) will not only increase IGF-I in the periphery, but will also increase IGF-I gene expression in liver and muscle tissue. It is also hypothesized that rbST treatment will increase gene expression of myosin in skeletal muscle tissue since more than half of the body mass of fish is comprised of muscle tissue. Our results suggest a difference in growth regulation in rainbow trout treated with exogenous somatotropin, as endogenous ST was unaffected by rbST treatment. This absence of a reduction in endogenous ST could be due to a different regulatory mechanism for extra-pituitary production of ST in rainbow trout or may result from a decrease in overall ST receptor numbers. Since muscle IGF-I mRNA was not affected and liver IGF-I mRNA levels were elevated by increased plasma IGF-I and rbST, it is suggested that ST and IGF-I act on muscle directly via endocrine means, as liver is the primary tissue producing IGF-I secreted into the periphery.
Technical Abstract: Many fish species, exhibit indeterminate growth throughout their lives. Recombinant bovine somatotropin (rbST) treatment increases growth rates of rainbow trout, and previous work with rbST treatment showed increased hyperplastic muscle growth. An experiment was conducted to examine the specific growth-promoting effects of rbST in rainbow trout. Sixty-six rainbow trout received an injection of either rbST suspended in sesame oil or sesame oil every 21 days beginning on day 0. Blood and tissue samples were collected on days 0, .5, 1, 3, 7, and 28 and assayed for changes in circulating hormones and steady-state gene expression levels. Rainbow trout somatotropin (rtST), rbST, and IGF-I in circulation were assayed by RIA. Gene expression levels were examined using real-time reverse-transcription polymerase chain reaction and Western blot assays. The rbST levels increased in circulation 12 hours after treatment and continued to increase after treatment. Recombinant bST treatment increased serum IGF-I levels one week after treatment, while endogenous ST was unaffected over time. Steady-state levels of muscle IGF-I mRNA were unaffected by rbST treatment, while steady-state liver IGF-I mRNA levels increased. Liver IGF-I mRNA increased 1 day post-treatment and remained elevated throughout the trial. Steady-state muscle myosin mRNA levels were unaffected by rbST treatment. These results suggest a reduction in the endogenous negative control feedback loop within the GH-IGF-I axis, as rtST was unaffected by increased circulating rbST and IGF-I, in contrast to an expected down-regulation of endogenous ST. It is also suggested that rbST acts on muscle growth via endocrine pathways, because local IGF-I mRNA was unaffected in muscle tissue but circulating IGF-I was increased.