TY - JOUR
T1 - Environmental estrogens inhibit growth of rainbow trout (Oncorhynchus mykiss) by modulating the growth hormone-insulin-like growth factor system
AU - Hanson, Andrea M.
AU - Kittilson, Jeffrey D.
AU - Martin, Lincoln E.
AU - Sheridan, Mark A.
N1 - Funding Information:
We would like to thank Heather Bergan, Whitney Carlson, Michael Caruso, Elizabeth Ellens, Evan Jones, Dillon Marquart, Lindsey Norbeck, and Chad Walock for their technical assistance. This work was supported by Grants from the US Geological Survey/North Dakota Water Commission and NSF ( IOS 0920116 ) to M.A. Sheridan; A. Hanson was supported by fellowships from the North Dakota Water Resources Research Institute and the NDSU Graduate School .
PY - 2014/1/5
Y1 - 2014/1/5
N2 - Although environmental estrogens (EE) have been found to disrupt a wide variety of developmental and reproductive processes in vertebrates, there is a paucity of information concerning their effects on organismal growth, particularly postembryonic growth. In this study, we exposed juvenile rainbow trout (Oncorhynchus mykiss) to 17β-estradiol (E2) β-sitosterol (βS), or 4- n-nonylphenol (NP) to assess the effects of EE on overall organismal growth and on the growth hormone-insulin-like-growth factor (GH-IGF) system. EE treatment significantly reduced food conversion, body condition, and body growth. EE-inhibited growth resulted from alterations in peripheral elements of the GH-IGF system, which includes multiple GH receptors (GHRs), IGFs, and IGF receptors (IGFRs). In general, E2, βS, and NP reduced the expression of GHRs, IGFs, and IGFRs; however, the effects varied in an EE-, tissue-, element type-specific manner. For example, in liver, E2 was more efficacious than either βS, and NP in reducing GHR expression, and the effect of E2 was greater on GHR 1 than GHR2 mRNA. By contrast, in gill, all EEs affected GHR expression in a similar manner and there was no difference in the effect on GHR1 and GHR 2 mRNA. With regard to IGF expression, all EEs reduced hepatic IGF1 and IGF2 mRNA levels, whereas as in gill, only E2 and NP significantly reduced IGF1 and IGF2 expression. Lastly, E2 and NP reduced the expression of IGFR1A and IGFR1B mRNA expression similarly in gill and red and white muscle, whereas βS had no effect on expression of IGFR mRNAs. These findings indicate that EEs disrupt post-embryonic growth by reducing GH sensitivity, IGF production, and IGF sensitivity.
AB - Although environmental estrogens (EE) have been found to disrupt a wide variety of developmental and reproductive processes in vertebrates, there is a paucity of information concerning their effects on organismal growth, particularly postembryonic growth. In this study, we exposed juvenile rainbow trout (Oncorhynchus mykiss) to 17β-estradiol (E2) β-sitosterol (βS), or 4- n-nonylphenol (NP) to assess the effects of EE on overall organismal growth and on the growth hormone-insulin-like-growth factor (GH-IGF) system. EE treatment significantly reduced food conversion, body condition, and body growth. EE-inhibited growth resulted from alterations in peripheral elements of the GH-IGF system, which includes multiple GH receptors (GHRs), IGFs, and IGF receptors (IGFRs). In general, E2, βS, and NP reduced the expression of GHRs, IGFs, and IGFRs; however, the effects varied in an EE-, tissue-, element type-specific manner. For example, in liver, E2 was more efficacious than either βS, and NP in reducing GHR expression, and the effect of E2 was greater on GHR 1 than GHR2 mRNA. By contrast, in gill, all EEs affected GHR expression in a similar manner and there was no difference in the effect on GHR1 and GHR 2 mRNA. With regard to IGF expression, all EEs reduced hepatic IGF1 and IGF2 mRNA levels, whereas as in gill, only E2 and NP significantly reduced IGF1 and IGF2 expression. Lastly, E2 and NP reduced the expression of IGFR1A and IGFR1B mRNA expression similarly in gill and red and white muscle, whereas βS had no effect on expression of IGFR mRNAs. These findings indicate that EEs disrupt post-embryonic growth by reducing GH sensitivity, IGF production, and IGF sensitivity.
KW - Environmental estrogens
KW - Growth hormone
KW - Insulin-like growth factor
UR - http://www.scopus.com/inward/record.url?scp=84891120909&partnerID=8YFLogxK
U2 - 10.1016/j.ygcen.2013.11.013
DO - 10.1016/j.ygcen.2013.11.013
M3 - Article
C2 - 24291304
AN - SCOPUS:84891120909
SN - 0016-6480
VL - 196
SP - 130
EP - 138
JO - General and Comparative Endocrinology
JF - General and Comparative Endocrinology
ER -