Energy-restricted diet during lactation programs ovarian growth factor and gonadotropin receptor expression in rats
نویسنده
چکیده
The goal of this study was to evaluate whether a maternal energy-restricted diet could program ovarian angiogenesis and growth factor and gonadotropin receptors expression in rats. After parturition, six Wistar rats with 6 pups each were randomly assigned to one of the following groups: control group (C), with free access to a standard laboratory diet containing 23% protein; and energy-restricted group (ER), receiving 60% of the amount consumed by the control group. After weaning, all female pups had free access to the standard laboratory diet until 90 days of age, when they were sacrificed during the proestrus stage. Blood was collected for further evaluation of serum estradiol levels. One ovary was stored at -80oC for RT-PCR analysis while the other one was paraffin embedded, sectioned at 5-μm thickness and processed by routine histological analysis for evaluation of vessel density. The ER group had a reduction in follicle stimulating hormone (C = 2.36 ± 0.21, ER = 0.97 ± 0.15, P < 0.001) and luteinizing hormone (C = 1.81 ± 0.11, ER = 0.74 ± 0.11, P < 0.0004) receptor expression. This group also had an increase in gene expression of basic fibroblast growth (C = 0.51 ± 0.07, ER = 0.72 ± 0.06, P < 0.04) and vascular endothelial growth factors (C = 0.82 ± 0.03, ER = 1.06 ± 0.08, P < 0.02). Estradiol serum concentration, vessel density, kinase-insert domain receptor, Fms-like tyrosine kinase-1 and fibroblast growth factor receptor-1 gene expressions were unchanged. The results indicated that a maternal energy-restricted diet during lactation programs the ovarian response to FSH, LH and angiogenic factors.
منابع مشابه
Maternal protein-energy and energy-restricted diets during lactation possibly could program folliculogenesis and the ovarian expression of leptin and its different isoform receptors in rats.
Both protein-energy and energy-restricted diets during lactation program the ovarian function of the rat offspring, leading to a reduction of folliculogenesis, possibly as the consequence of the altered expression of leptin and its isoform receptor genes.
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