Effects of Perinatal Maternal Food Restriction on Pituitary-Gonadal Axis and Plasma Leptin Level in Rat Pup at Birth and Weaning and on Timing of Puberty

Abstract

The effects of maternal 50% food restriction (FR) during the last week of gestation and/or lactation on pituitary-gonadal axis (at birth and weaning), on circulating levels of leptin (at weaning), and on the onset of puberty have been determined in rats at birth and at weaning. Maternal FR during pregnancy has no effect at term on the litter size, on the basal level of testosterone in male pups, and on the drastic surge of circulating testosterone that occurs 2 h after birth. At weaning, similar retardation of body growth is observed in male and female pups from mothers exposed to FR. This undernutrition induces the most drastic effects when it is performed during both gestation and lactation or during lactation alone. Drastic retardation of testicle growth with reduction of cross-sectional area and intratubular lumen of the seminiferous tubules is observed in male pups from mothers exposed to undernutrition during both gestation and lactation or during lactation alone. Maternal FR during the perinatal period reduces circulating levels of FSH in male pups without affecting LH and testosterone concentrations. Maternal FR does not affect circulating levels of LH, estradiol, and progesterone in female pups. Female pups from mothers exposed to FR during both gestation and lactation show a significant increase of plasma FSH as well as a drastic retardation of ovarian growth. The follicular population was also altered. The number of antral follicles of small size (vesicular follicles) was increased, although the number of antral follicles of large size (graafian follicles) was reduced. Maternal FR occurring during both late gestation and lactation (male and female pups), during lactation alone (male and female pups), or during late gestation (female pups) induces a drastic reduction of plasma leptin and fat mass in pups at weaning. The onset of puberty is delayed in pups of both sexes from mothers exposed to FR during lactation and during both gestation and lactation. In conclusion, these data demonstrate that a perinatal growth retardation induced by maternal FR has long-term consequences on both size and histology of the genitals, on plasma gonadotropins and leptin levels, on fat stores at weaning, and on the onset of puberty.

Effects of maternal nuclear genome on the timing of puberty in mice offspring

“…Androgens, corticosteroids and thyroid hormones are among the maternally derived hormones with significant roles during embryonic development in vertebrates. Previous studies showed that ingredient variations in the maternal diet during pregnancy and lactation could affect the pubertal status of female progeny (Cooper et al 1996, Lumey & Stein 1997, Magnusson et al 1999, Adair 2001, Leonhardt et al 2003, Figure 4 Growth curves of two inbred strains of male mice and the direct and reciprocal Fl crosses. N indicates the number of pups included.…”

Developmental variations in environmental influences including endocrine disruptors on pubertal timing and neuroendocrine control: Revision of human observations and mechanistic insight from rodents

“…Maternal food restriction (Leonhardt et al, 2003;Iwasa et al, 2010) or uterine artery ligation (Engelbregt et al, 2000) are associated with late vaginal opening or first estrus. Some authors have reported no effect of maternal food restriction on pubertal development while a single study (Sloboda et al, 2009) found an acceleration of pubertal onset.…”

Delay in the onset of puberty of intrauterine growth retarded female rats cannot be rescued with hypernutrition after birth

“…The age of vaginal opening (VO) and the first estrous was delayed, ovarian and testicular growth were drastically retarded and ovulation rate was lower in the undernourished during prenatal period by several kind of animal models in uterine artery ligation, prenatal food or protein restriction and subjected to glucocorticoid overexposure [6][7][8][9][10]. These reports suggest that there is an association between restricted fetal growth and the programming of disease after birth [11][12][13].…”