Abstract

The maternal nutritional status is essential to the health and well-being of the fetus. Maternal protein restriction during the perinatal stage causes sperm alterations in the offspring that are associated with epididymal dysfunctions. Vascular endothelial growth factor (VEGF) and its receptor, VEGFr-2, as well as aquaporins (AQPs) are important regulators of angiogenesis and the epididymal microenvironment and are associated with male fertility. We investigated the effects of maternal protein restriction on epididymal angiogenesis and AQP expression in the early stages of postnatal epididymal development. Pregnant rats were divided into two experimental groups that received either a normoprotein (17% protein) or low-protein diet (6% protein) during gestation and lactation. At postnatal day (PND)7 and PND14, male offspring were euthanized, the epididymides were subjected to morphometric and microvascular density analyses and to VEGF-A, VEGF-r2, AQP1 and AQP9 expression analyses. The maternal low-protein diet decreased AQP9 and VEGFr-2 expression, decreased epididymal microvascularity and altered the morphometric features of the epididymal epithelium; no changes in AQP1 expression were observed at the beginning of postnatal epididymal development. Maternal protein restriction alters microvascularization and affects molecules involved in the epidydimal microenvironment, resulting in morphometric alterations related to a delay in the beginning of epididymis postnatal development.

Highlights

  • Studies have revealed potential factors that increase the risks of diseases during the developmental period unpublished data [1,2,3]

  • The levels of VEGFa were increased and those of VEGF receptor 2 (VEGFr-2) were decreased in LP animals compared with NP animals at PND7 (Figure 2)

  • In the present study,AQP9 we showed that a maternal low-protein diet during gestation and lactation was able to decrease and VEGFr-2 expression while enhancing expression, changing wasthe able to decrease

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Summary

Introduction

Studies have revealed potential factors that increase the risks of diseases during the developmental period unpublished data [1,2,3]. These studies support the developmental origins hypothesis, which is based on the interaction between early developmental plasticity and environmental factors, and studies have been conducted to determine the mechanisms by which these factors may affect health and disease later in life [4,5]. The genome is evolutionarily and chemically very stable, so environmental factors generally do not cause genomic changes in DNA sequences. These factors may cause hereditary changes through manipulation independent of DNA sequence, thereby changing the epigenome. Male infertility has been shown to be associated with congenital defects

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