Analysis of the mechanism of skeletal deformity in fish larvae using a vitamin A-induced bone deformity model

Vitamin A (VA) is an essential nutrient in fish. VA is involved in a large spectrum of biological processes. One of the most important functions of VA is to control embryonic development in animals. In mammals, organogenesis is completed during embryogenesis. In contrast, most marine fish larvae are in a comparatively immature state at hatching and undergo organogenesis during the exogenous feeding stage. This developmental feature of marine fish larvae requires appropriate control of the nutritional composition of the diet to support normal skeleton development. Nutrient deficiency or imbalance results in skeletal deformities that are often recognized in hatchery-reared fish. However, the etiology and precise mechanism of such skeletal deformities are unknown, which makes it difficult to achieve an effective prevention protocol in hatcheries. Skeletal deformities induced by excess VA are a popular model for studying the development of skeletons in fish larvae. Several studies suggest the importance of retinoic acid receptor (RAR) and retinoid X receptor (RXR) pathways in skeletogenesis in fish. This paper reviews the current understanding of VA-induced skeletal deformities and recent progress in this area and proposes future perspectives for model studies.