Impact of maternal overweight on the sexual maturity of male offspring in rats.

The aims of the present work were to study the effect of maternal overweight on both the count and quality of sperm of the offspring and to assess whether this maternal condition is able to alter testicular integrity and spermatogenic process. To this end, male offspring from rats fed a standard (OSD) or cafeteria (OCD) diet were used. Body and testis weight, length, preputial separation and ano-genital distance (AGD) were recorded and testes were removed at 60 days of age. In addition, the number of germ, Leydig and Sertoli cells, spermatogenesis and sperm integrity were examined. The OCD rats were divided into two groups: offspring from rats with 25% and≥35% of overweight (OCD25 and OCD35, respectively). Both OCD groups showed higher body and testis weight, higher length, and greater AGD than OSD rats. OCD25 also showed early preputial separation and OCD35 exhibited a high level of testosterone with normal glycemia. Both OCD25 and OCD35 rats had a lower number of spermatozoa and Leydig cells than OSD rats, and OCD35 also exhibited a lower number of spermatogonia and Sertoli cells than OSD rats. In addition, both OCD groups exhibited lower number of sperm cells with normal morphology and sperm motility, and OCD35 showed changes in both the seminiferous epithelium and spermatogenic process. These results suggest that maternal overweight severely affects the reproductive capacity of male offspring, likely leading to a subfertility condition and a premature reduction of the reproductive life span.

Evaluation of sodium arsenite exposure on reproductive competence in pregnant and postlactational dams and their offspring.

We investigated arsenite exposure on the reproductive axis of dams (during pregnancy and at cyclicity resumption) and their offspring. Pregnant rats were exposed to 5 (A5) or 50ppm (A50) of sodium arsenite in drinking water from gestational day 1 (GD1) until sacrifice at GD18 or two months postpartum. Offspring were exposed to the same treatment as their mothers from weaning to adulthood. A50-pregnant rats gained less weight, showed increased testosterone and estradiol but pregnancy was unaffected. After lactation, arsenic-exposed dams presented compromised cyclicity, decreased estradiol, increased follicle-stimulating hormone (FSH), less preovulatory follicles and presence of ovarian cysts, suggesting impaired reproduction. A50-offspring presented lower body weight; A50-female-offspring showed elevated gonadotropin releasing hormone (GnRH), FSH and testosterone, while A50-males showed diminished GnRH/FSH, but normal testosterone. We conclude that arsenite at the present exposure levels did not compromise pregnancy outcome while it negatively affected reproductive physiology in postpartum dams and their offspring.

Arsenite in drinking water produces glucose intolerance in pregnant rats and their female offspring.

Drinking water is the main source of arsenic exposure. Chronic exposure has been associated with metabolic disorders. Here we studied the effects of arsenic on glucose metabolism, in pregnant and post-partum of dams and their offspring. We administered 5 (A5) or 50 (A50) mg/L of sodium arsenite in drinking water to rats from gestational day 1 (GD1) until two months postpartum (2MPP), and to their offspring from weaning until 8 weeks old. Liver arsenic dose-dependently increased in arsenite-treated rats to levels similar to exposed population. Pregnant A50 rats gained less weight than controls and recovered normal weight at 2MPP. Arsenite-treated pregnant animals showed glucose intolerance on GD16-17, with impaired insulin secretion but normal insulin sensitivity; they showed dose-dependent increased pancreas insulin on GD18. All alterations reverted at 2MPP. Offspring from A50-treated mothers showed lower body weight at birth, 4 and 8 weeks of age, and glucose intolerance in adult females, probably due to insulin secretion and sensitivity alterations. Arsenic alters glucose homeostasis during pregnancy by altering beta-cell function, increasing risk of developing gestational diabetes. In pups, it induces low body weight from birth to 8 weeks of age, and glucose intolerance in females, demonstrating a sex specific response.