Maternal obesity disturbs the postnatal development of gonocytes in the rat without impairment of testis structure at prepubertal age

Abstract

In this study, we evaluated whether maternal obesity (MO) affects testis development and gonocyte differentiation in the rat from 0.5 to 14.5 postnatal days. Male Wistar rats were used at 0.5, 4.5, 7.5, and 14.5 days post partum (dpp). These rats were born from obese mothers, previously fed with a high-fat diet (20% saturated fat), for 15 weeks, or normal mothers that had received a balanced murine diet (4% lipids). MO did not affect testis weight or histology at birth but changed the migratory behavior of gonocytes. The density of relocated cells was higher in MO pups at 0.5 dpp, decreased at 4.5 dpp, and differed from those of control pups, where density increased exponentially from 0.5 to 7.5 dpp. The numerical density of gonocytes within seminiferous cords did not vary in MO, in relation to control neonates, for any age considered, but the testis weight was 50% lower at 4.5 dpp. A wide variation in plasmatic testosterone and estrogen levels was observed among the groups during the first week of age and MO pups exhibited higher steroid concentrations at 4.5 dpp, in comparison with controls. At this age, higher estrogen levels of MO pups impaired the gonocyte proliferation. At 7.5 dpp, the testicular size and other parameters of gonocyte development are retrieved. In conclusion, MO and saturated lipid diets disturb gonocyte development and sexual steroid levels during the first days of life, with recovery at prepubertal age.

Differential ontogenetic exposure to obesogenic environment induces hyperproliferative status and nuclear receptors imbalance in the rat prostate at adulthood

“…However, the prostate hypertrophy observed in G group, which did not exhibit elevated cell proliferation but showed higher stromal ERα, raises the question whether altered intrauterine hormonal and nutritional milieu due to maternal obesity affect the developmental programming of the gland altering the sensitivity to steroids in perinatal periods and impacting prostate development in the first weeks of age. This possibility is supported by previous results from our laboratory about testicular development indicating that pups from mothers subjected to the same OE utilized here exhibited low testosterone and high estrogen levels in the first postnatal days . The expression of several nuclear receptors during neonatal e pubertal differentiation after maternal OE will clarify this question.…”

Impact of maternal hyperlipidic hypercholesterolaemic diet on male reproductive organs and testosterone concentration in rabbits

“…At D7.5, there was no difference between the groups again. 10 These studies used different species (sheep, rats) and the dams were overweight, whereas they have increased body fat in the present study. Moreover, the rabbit is a more appropriate model for high-fat nutrition and to assess the effect of developmental programming on reproductive functions.…”

A paternal environmental legacy: Evidence for epigenetic inheritance through the male germ line

“…A high-fat diet of the parents before and during mating results in offspring with increased body-fat accumulation, increased weight gain, and altered expression of lipoprotein lipase and leptin in adipose tissues [108]. Maternal obesity in rat disturbs postnatal steroid levels and development of male germ cells [109]. Paternal food deprivation in male mice before conception leads to offspring with impaired glucose metabolism [25].…”