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Effects of chronic cysteamine treatment on growth enhancement and insulin-like growth factor I and II mRNA levels in common carp tissues

Published online by Cambridge University Press:  08 March 2007

Margaret C. L. Tse
Affiliation:
Department of Biochemistry, The Chinese University of Hong Kong, Sha Tin, New Territories, Hong Kong SAR, China
Christopher H. K. Cheng
Affiliation:
Department of Biochemistry, The Chinese University of Hong Kong, Sha Tin, New Territories, Hong Kong SAR, China
King Ming Chan*
Affiliation:
Department of Biochemistry, The Chinese University of Hong Kong, Sha Tin, New Territories, Hong Kong SAR, China
*
*Corresponding author: Dr K. M. Chan, fax +852 26035123, email kingchan@cuhk.edu.hk
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Abstract

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Insulin-like growth factors (IGF) belong to a family of growth factors with structural homology to proinsulin. In our previous studies, we found that both IGF-I and IGF-II gene expression showed growth hormone (GH) dependence in the brain and liver of juvenile common carp when treated in vivo with GH for a short time. This present work aimed to study the effects of both the short-term and long-term GH induction of IGF gene expression using cysteamine (CSH) and fasting/re-feeding. CSH is an agent that can deplete somatostatin to increase circulating GH level. IGF mRNA levels in the flesh (muscle) and liver of common carp were determined using real-time PCR.

The chronic treatment of common carp with CSH was carried out for 63d, with growth enhancement of the treated fish noted. Hepatic IGF-I and IGF-II mRNA levels increased in a dose-dependent manner with short-term CSH treatment, whereas IGF-I decreased and IGF-II increased in the liver after chronic CSH treatment. IGF-I and IGF-II mRNA levels in muscle were found to be elevated with the high-dose, long-term CSH treatment. Under the experimentally induced catabolic states of fasting, both hepatic IGF-I and IGF-II gene expression were significantly reduced, whereas they showed no change in muscle. After re-feeding, the hepatic expression of IGF-I in liver and muscle rebounded significantly. The hepatic IGF-II expression level showed no rebound after re-feeding, but the IGF-II level in muscle rebounded to the level of the fed group after re-feeding.

Type
Research Article
Copyright
Copyright © The Nutrition Society 2006

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