Maternal malnutrition during lactation affects folliculogenesis, gonadotropins, and leptin receptors in adult rats.

OBJECTIVE: The goal of this study was to evaluate if maternal malnutrition during lactation could possibly program folliculogenesis, the ovarian expression of gonadotropins, leptin, and their receptors. METHODS: At parturition, dams were randomly assigned to a control group (C), with free access to a standard laboratory diet containing 23% protein, and a protein-energy-restricted group (PER), with free access to an iso-energy and protein-restricted diet containing 8% protein. After weaning, all female pups had free access to the standard laboratory diet until 90 d of age when they were euthanized in the diestrum stage. RESULTS: Maternal malnutrition caused decreases in the number of primordial (C 6.60 ± 0.24, PER 5.20 ± 0.20, P = 0.01), primary (C 5.80 ± 0.66, PER 4.00 ± 0.31, P = 0.04), and Graafian (C 2.18 ± 0.29, PER 1.08 ± 0.37, P = 0.05) follicle numbers. Maternal malnutrition led to a significant decrease in the aromatase mRNA expression (C 0.536 ± 0.008, PER 0.353 ± 0.041, P = 0.01) follicle-stimulating hormone receptor (C 1.25 ± 0.17, PER 0.75 ± 0.02, P = 0.04), luteinizing hormone receptor (C 0.93 ± 0.09, PER 0.54 ± 0.10, P = 0.03), leptin (C 0.55 ± 0.03, PER 0.42 ± 0.03, P = 0.04), Ob-R (C 1.05 ± 0.12, PER 0.64 ± 0.07, P = 0.03), and Ob-Rb (C 1.34 ± 0.21, PER 0.47 ± 0.10, P = 0.02) transcripts when compared with C. CONCLUSION: Maternal malnutrition during lactation modulates folliculogenesis and the expression of the different isoforms of leptin and gonadotropin receptors and the aromatase enzyme. This probably is a consequence of alterations in perinatal leptin concentrations that may play a crucial role in determining the occurrence of long-term metabolic changes.