Maternal malnutrition during lactation alters the folliculogenesis and gonadotropins and estrogen isoforms ovarian receptors in the offspring at puberty

In this study, we aimed to evaluate whether maternal malnutrition during lactation alters the folliculogenesis and the expression of the gonadotropins and estrogen isoforms ovarian receptors in the offspring at puberty. At parturition, darns were randomly assigned to the following groups: control (C) group, with free access to a standard laboratory diet containing 23% protein and protein-energy-restricted (PER) group, with free access to an isoenergy and protein-restricted diet containing 8% protein. After weaning, the female pups had free access to standard laboratory diet. The maternal malnutrition caused a significant increase in the number of preantral (C = 13.72 +/- 2.87; P.ER=26.36 +/- 3.03, P < 0.01) and small antral follicles (C = 9.32 +/- 1.35; PER = 17.64 +/- 2.33, P < 0.01) and decrease in the number of primordial (C = 11.72 +/- 1.37; PER = 3.92 +/- 0.60, P < 0.01) and Graafian follicles (C = 1.84 +/- 0.21; PER = 0.96 +/- 0.11, P < 0.01), and corpus luteum (C = 2.00 +/- 0.28; PER = 0.80 +/- 0.31, P < 0.01). The estradiol serum concentration was significantly higher (C = 67.86 +/- 4.39; PER = 83.29 +/- 2.68, P < 0.05) while testosterone serum concentration did not show statistical difference (C = 0.09 +/- 0.02; PER = 0.11 +/- 0.01, P > 0.05) in the PER group. In relation to the receptors expression, maternal malnutrition led to a significant increase in the amount of Fshr (C = 0.89 +/- 0.04; PER = 1.07 +/- 0.03, P < 0.05) and Lhcqr (C = 0.87 +/- 0.15; PER = 1.33 +/- 0.08, P < 0.05) transcripts and a significant decrease in the amount of Ar (C = 0.59 +/- 0.006; PER = 0.13 +/- 0.080, P < 0.05), ER alpha (Esr1) (C = 3.33 +/- 0.71; PER = 0.74 +/- 0.50, P < 0.05), ER beta 1 (Esr2) (C = 1.33 +/- 0.06; PER = 0.49 +/- 0.36, P < 0.05), and Ek beta 2 (Esr2) (C = 3.28 +/- 0.60; PER = 0.62 +/- 0.34, P < 0.05) transcripts. In conclusion, perinatal maternal malnutrition can directly affect folliculogenesis at puberty probably as a consequence of changes in the ovarian expression of gonadotropins, androgen and estrogens isoforms receptors. Long-term sexual alterations could be expected in this experimental model, since a reduction in the primordial follicle number is observed, which can result in a decrease in the reproductive lifetime and in earlier termination of breeding capacity.