Humans and animals adapt to space flight conditions. However, the adaptive changes of fully formed organisms differ radically from the responses of vertebrate embryos, foetuses, and larvae to space flight. Development is associated with active cell proliferation and the formation of organs and systems. The instability of these processes is well known. Over 20 years has passed since the last systematic experiments on vertebrate reproduction and development in space flight. At the same time, programs are being prepared for the exploration of Mars and the Moon, which justifies further investigations into space flight’s impact on vertebrate development. This review focuses on various aspects of reproduction and early development of vertebrates in space flights. The results of various experiments on fishes, amphibians, reptiles, birds and mammals are described. The experiments in which our team took part and ontogeny of the vertebrate nervous and special sensory systems are considered in more detail. Possible causes of morphological changes are also discussed. Research on evolutionarily and taxonomically different models can advance the understanding of reproduction in microgravity. Reptiles, in particular, geckos, due to their special features, can be a promising object of space developmental biology.

Alterations of pancreatic islet cell phenotypes are well established in diabetic conditions and considered to be one of the possible causes of insulin deficiency. However, there is limited information about alterations of islet cell phenotypes in opposite metabolic conditions such as hypoglycemia in infants with congenital hyperinsulinism (CHI). Surgical biopsies of the pancreas from six infants with diffuse CHI and five infants with focal CHI were examined using double immunofluorescence with antibodies against insulin, glucagon and the key transcriptional factor responsible for β-cell differentiation and maturation—PDX1. The phenotypes of cells within the pancreatic islets in diffuse CHI and within the focus in focal CHI were compared to those in unaltered pancreatic islets located outside the focus. In diffuse CHI, the proportion of bi-hormonal insulin+/glucagon+ cells was increased. Additionally, an increase in the proportion of insulin+ cells lacking PDX1 was observed in diffuse CHI and within the focus. It can be assumed that alterations of the phenotype of β-cells may occur under hypoglycemic conditions, but the role of islet cell plasticity in infants with CHI remains to be established.