Nutritional and developmental regulation of insulin-like growth factors in fish

Abstract

The insulin-like growth factors (IGF) are evolutionarily ancient growth factors present in all vertebrates. The central importance of IGF for normal development and growth has been illustrated by the severe growth-retarded phenotype exhibited by IGF-I, IGF-II or IGF-I receptor "knockout" mice. Although we know much about the gross effects of IGF on the overall size of the fetus and the clinical manifestations that result from fetal and neonatal deficiency of IGF (i.e., severe growth retardation leads to dwarfism), very little is known about the in vivo actions of IGF during embryogenesis at the cellular and molecular levels. Most research on the developmental role of IGF has relied on rodent models, and attempts to elucidate the molecular and cellular basis of IGF actions have been hampered by the inaccessibility of the mammalian fetus enclosed in the uterus. During the past decade, there has been growing support for the concept that the IGF have been highly conserved in all vertebrates. Both IGF-I and IGF-II are present in fish, and their structures are highly conserved. Human and fish IGF-I are equally potent in mammalian and fish bioassay systems. Insulin-like growth factor mRNA is found in all life stages of fish, ranging from unfertilized egg to adult. The temporal and spatial expression patterns of fish IGF-I seem to be similar to those in mammals. Nutritional status and growth hormone both have a profound effect on IGF-I expression in fish, as they do in mammals. These features suggest that the IGF system is highly conserved between teleost fish and mammals. Because fish embryos develop externally, they provide excellent animal models for understanding the regulatory roles of IGF, IGF receptor and IGF-binding proteins in vertebrate embryonic development. Current research on the developmental and nutritional roles of IGF in fish will undoubtedly contribute to knowledge of the basic physiology of vertebrates in general.