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Placental HSD2 Expression and Activity Is Unaffected by Maternal Protein Consumption or Gender in C57BL/6 Mice

机译:C57BL / 6小鼠的母体蛋白质消耗或性别不会影响胎盘HSD2的表达和活性。

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摘要

The placenta acts as a physiological barrier, preventing the transfer of maternal glucocorticoids to the developing fetus. This is accomplished via the oxidation, and subsequent inactivation, of endogenous glucocorticoids by the 11-β hydroxysteroid dehydrogenase type 2 enzyme (HSD2). Maternal protein restriction during pregnancy has been shown to result in a decrease in placental HSD2 expression and fetal glucocorticoid overexposure, especially late in gestation, resulting in low birth weight and “fetal programming” of the offspring. This dietary intervention impairs fetal growth and cardiovascular function in adult C57BL/6 offspring, but the impact on placental HSD2 has not been defined. The goal of the current study was to examine the effects of a maternal low-protein diet (18% versus 9% protein) on placental HSD2 gene expression and enzyme activity in mice during late gestation. In contrast to previous studies in rats, a maternal low-protein diet did not affect HSD2 protein or enzyme activity levels in the placentas of C57BL/6 mice and this was irrespective of the gender of the offspring. These data suggest that the effects of maternal protein restriction on adult phenotypes in C57BL/6 mice depend upon a mechanism that may be independent of placental HSD2 or possibly occurs earlier in gestation.
机译:胎盘充当生理屏障,阻止母体糖皮质激素转移至发育中的胎儿。这是通过11-β羟类固醇脱氢酶2型酶(HSD2)氧化内源性糖皮质激素并随后使其失活来实现的。孕妇在怀孕期间的蛋白质限制已显示可导致胎盘HSD2表达降低和胎儿糖皮质激素过度暴露(尤其是在妊娠后期),从而导致低出生体重和后代的“胎儿编程”。这种饮食干预会损害成年C57BL / 6后代的胎儿生长和心血管功能,但对胎盘HSD2的影响尚未明确。本研究的目的是检查孕晚期母体低蛋白饮食(18%比9%的蛋白质)对小鼠胎盘HSD2基因表达和酶活性的影响。与之前的大鼠研究相比,母体低蛋白饮食不会影响C57BL / 6小鼠胎盘中的HSD2蛋白或酶活性水平,而与后代的性别无关。这些数据表明母体蛋白质限制对C57BL / 6小鼠中成年表型的影响取决于一种机制,该机制可能与胎盘HSD2无关或可能在妊娠早期发生。

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