Meeting Abstract
The growth hormone (GH) / insulin-like growth factor-1 (IGF-1) axis regulates somatic growth in vertebrates by activating growth-promoting pathways in almost all tissues. Nutritional stress in the form of reduced food quantity or quality has been shown to inhibit growth in part by blocking GH induction of hepatic IGF-1 production, but the mechanism(s) of that inhibition are not well understood. Here, we examined how food deprivation (fasting) affected GH induction of liver IGF-1 production in juvenile gopher rockfish, Sebastes carnatus. Rockfish were maintained under conditions of either feeding (9% mass fed per g fish mass) or fasting for 14 d, and then injected intraperitoneally with recombinant seabream GH (2 μg per 1 g mass) or saline control. Liver IGF-1 mRNA levels were generally lower in fasted fish than in fed fish, and GH upregulated hepatic IGF-1 mRNAs 2.2-fold in fed fish, but only 1.4-fold in fasted fish. Liver mRNA levels for two proteins that mediate downstream effects of GH in the liver, janus kinase 2 (JAK2) and signal transducer and activator of transcription 5β (STAT5β), did not vary with fasting or GH treatment. However, transcripts encoding hepatocyte nuclear factor-3β (HNF3β), a transcription factor linked to IGF-1 expression, were at higher abundance both in fed fish and in fish receiving GH. Transcripts encoding IGF binding protein acid labile subunit (IGFALS), which enables IGF-1 interactions with IGF binding proteins, were unaffected by fasting, but increased in both fed and fasted fish treated with GH. These findings point to the downregulation of distinct pathways involving HNF3&beta and IGFALS as possible contributors inhibiting liver IGF-1 production under conditions of nutritional stress.
