This finding is consistent with the high renin and AT1r expressions observed in the present study. Activation of the RAS may play a significant role in the development of mechanisms that lead to kidney damage. After kidney damage occurs, chronic renal disease progresses through a cycle that passes the damage from lost or damaged nephrons to healthy nephrons. Two hypotheses are currently proposed to explain the progression of chronic renal disease. The results of the present study are consistent with the “overload hypothesis”. This hypothesis suggests that AB1010 VEGFR/PDGFR inhibitor structural and functional adaptations are associated with glomerular hypertension, hyperfiltration, and hypertrophy partially compensated for nephron losses. Podocin provides the structural organization of the slit diaphragm and the regulation of filtration function and seems to be involved in the alteration of the glomerular basement membrane. Nephrin is expressed late in the process of podocyte differentiation and is a locus for the formation of the slit diaphragm, foot process maintenance and physical integrity in vivo, but it is dispensable for cell survival and has little impact on gene regulation during glomerular development. Nephrin does not affect podocyte apoptosis and gene expression patterns. In the present study, vitamin D restriction during nephrogenesis reduced podocin expression in the F1 generation from weaning until six months of age but not in the F2 generation. Such effects should be evaluated because podocin serves in the structural organization of the slit diaphragm and the regulation of its filtration function. Although the mature animals did not show significant proteinuria, maternal vitamin D deficiency altered podocin expression in the F1 generation from weaning until six months of age, but not in the F2 generation. Intense maternal protein restriction, for example, leads to chronic diseases in adult life, affecting both the F1 and F2 generations, and reaching even the F3 generation. Part of the explanation seems to be decreased global methylation in these offspring. The present study has certain limitations. The major aim of the study was to investigate glomerular development and renal structure at birth, 10 days and adulthood in mice born to mothers fed a diet restricted in vitamin D. Although, we examined other variables, such as body mass and 24 h urine, the present study was not designed to investigate renal functional and metabolic consequences but rather was designed to answer the question of whether there were structural, glomerular alterations or transgenerational effects. Further studies are necessary to clarify the impact of maternal vitamin D restriction on the renal function of offspring. Furthermore, the literature shows some relationship between vitamin D deficiency and adipose tissue development, and other studies should evaluate such effects, and the transgenerational effects. In conclusion, the present findings provide insight into the relationship between maternal vitamin D deficiency and the occurrence of a greater number of glomeruli in offspring. Maternal vitamin D deficiency is accompanied by changes in the renal expression of podocin, renin and AT1 receptors, and it delays the maturity of the glomeruli, by extending nephrogenesis. These findings are more pronounced in F1 progeny, but F2 progeny are also affected. Gastric cancer is the fourth most common malignancy in the world and the second leading cause of cancer death in both sexes worldwide. The highest mortality rates are estimated in Eastern Asia. The 5-year survival rate for gastric cancer is less than 20%–25% in the USA, Europe and China.