1 Department of Obstetrics and Gynecology, Yamagata University Faculty of Medicine , Yamagata, Japan .
2 Osaka Medical Center and Research Institute for Maternal and Child Health , Izumi, Osaka, Japan .
J Womens Health (Larchmt). 2018 Jan;27(1):99-106. doi: 10.1089/jwh.2016.6301. Epub 2017 Aug 17.
This study aimed to evaluate differences in oxidative stress of visceral fat between premenopausal and postmenopausal women and clarify the antioxidant effect of estrogen on adipocytes.
Abdominal subcutaneous and omental visceral adipose tissues were obtained from 38 patients who underwent gynecological surgery. We measured the sizes of the adipocytes and evaluated the lipid peroxidation levels in the adipose tissues. We investigated whether estrogen inhibited the intracellular reactive oxygen species (ROS) production that was induced by hydrogen peroxide (HO) in 3T3-L1 adipocytes.
The visceral adipocytes were 1162.4 μm and 1881.9 μm in premenopausal and postmenopausal women, respectively; hence they were significantly larger in the latter (p < 0.05). The lipid peroxidation levels were 46.7 nmoL/mg protein in premenopausal women and 99.6 nmoL/mg protein in postmenopausal women; hence the lipid peroxidation levels were significantly higher in the latter (p < 0.05). Estradiol (E2) significantly reduced the intracellular ROS levels that were induced by H2O2 in 3T3-L1 adipocytes (p < 0.01). We determined that E2 significantly increased the expression of nuclear factor erythroid 2-related factor 2 (NRF2)-dependent antioxidant genes, heme oxygenase-1 (HO-1), NAD(P)H:quinone oxidoreductase 1 (NQO1), and the glutamate-cysteine ligase (GCL) modifier subunit genes, in 3T3-L1 adipocytes (p < 0.01).
Oxidative stress in the visceral fat is higher in postmenopausal women. The expression of the antioxidant genes HO-1, NQO1, and GCL was upregulated by estrogen in 3T3-L1 adipocytes. Hence, estrogen may act as an antioxidant in the adipose tissues of premenopausal women.
本研究旨在评估绝经前后女性内脏脂肪的氧化应激差异，并阐明雌激素对脂肪细胞的抗氧化作用。
本研究从 38 例行妇科手术的患者中获取了腹部皮下和网膜内脏脂肪组织。我们测量了脂肪细胞的大小，并评估了脂肪组织中的脂质过氧化水平。我们研究了雌激素是否能抑制 3T3-L1 脂肪细胞中过氧化氢（H2O2）诱导的细胞内活性氧（ROS）的产生。
绝经前和绝经后女性的内脏脂肪细胞分别为 1162.4 μm 和 1881.9 μm，后者显著大于前者（p<0.05）。绝经前女性的脂质过氧化水平为 46.7 nmoL/mg 蛋白，绝经后女性为 99.6 nmoL/mg 蛋白，后者显著高于前者（p<0.05）。雌二醇（E2）显著降低了 3T3-L1 脂肪细胞中 H2O2 诱导的细胞内 ROS 水平（p<0.01）。我们发现，E2 显著增加了 3T3-L1 脂肪细胞中核因子红细胞 2 相关因子 2（NRF2）依赖性抗氧化基因血红素加氧酶-1（HO-1）、NAD（P）H：醌氧化还原酶 1（NQO1）和谷氨酸-半胱氨酸连接酶（GCL）修饰亚基基因的表达（p<0.01）。
绝经后女性的内脏脂肪氧化应激更高。雌激素在 3T3-L1 脂肪细胞中上调了抗氧化基因 HO-1、NQO1 和 GCL 的表达。因此，雌激素可能在绝经前女性的脂肪组织中发挥抗氧化作用。
