Oxygen and embryonic growth: the role of insulin-like growth factor signaling

•Oxygen controls embryonic growth by modifying Igf-system in vertebrates.•Hypoxia limits Igf-action via Hif-mediated igfbp1a/b overexpression.•Re-oxygenation after hypoxia induces growth spurt termed catch-up growth.•Igf-Mapk pathway and NCCs are keys for the re-oxygenation induced catch-up growth. Oxygen is indispensable for the efficient release of chemical energy from nutrient molecules in cells. Therefore, the local oxygen tension is one of the most critical factors affecting physiological processes. In most viviparous species, many pathological conditions result in abnormal oxygen tension in the uterus, which modifies the growth and development of the fetus. Insulin-like growth factor (IGF/Igf) is one of the most important hormones for the regulation of somatic growth in animals. Changes in oxygen levels modulate the activity of the IGF/Igf signaling system, which in turn regulates the embryonic growth rate. In general, there are serious difficulties associated with monitoring and studying rodent embryos in utero. The zebrafish is a convenient experimental model to study the relationship between embryonic growth and environmental conditions. Most importantly, the fish model makes it possible to rapidly evaluate embryonic growth and development under entirely controlled environments without interfering with the mother organism. In this review, firstly an overview is given of the fluctuation of environmental oxygen, the IGF-system, and the advantages of the zebrafish model for studying embryonic growth. Then, the relationships of dynamic environmental oxygen and embryonic growth rate are outlined with a specific focus on the changes in the IGF/Igf-system in the zebrafish model. This review will shed light on the fine-tuning mechanisms of the embryonic IGF/Igf-system under different oxygen levels, including constant normoxia, hypoxia, and re-oxygenation.