ABSTRACT

Our group recently documented that male mice containing a deletion for one copy of the glutaredoxin-2 (Grx2) gene were completely protected from developing diet-induced obesity (DIO).

Objectives: Here, we conducted a similar investigation but with female littermates.

Results: In comparison to our recent publication using male mice, exposure of WT and GRX2+/- female mice to a HFD from 3-to-10 weeks of age did not induce any changes in body mass, circulating blood glucose, food intake, hepatic glycogen levels, or abdominal fat pad mass. Examination of the bioenergetics of muscle mitochondria revealed no changes in the rate of superoxide ($O_2^{\bullet -}$)/hydrogen peroxide (H₂O₂) or O₂ consumption under different states of respiration or alterations in lipid peroxidation adduct levels regardless of mouse strain or diet. Additionally, we measured the bioenergetics of mitochondria isolated from liver tissue and found that partial loss of GRX2 augmented respiration but did not alter ROS production.

Discussion: Overall, our findings demonstrate there are sex differences in the protection of female GRX2+/- mice from DIO, fat accretion, intrahepatic lipid accumulation, and the bioenergetics of mitochondria from muscle and liver tissue.

摘要

我们的小组最近记录到，含有一个拷贝的谷氧还蛋白-2 (Grx2)基因缺失的雄性小鼠完全受到保护，不会发生饮食诱导的肥胖 (DIO)。

目标：在这里，我们进行了类似的调查，但调查对象是雌性同窝仔。

结果：与我们最近使用雄性小鼠发表的文章相比，将 WT 和 GRX2+/- 雌性小鼠从 3 至 10 周龄暴露于 HFD 不会引起体重、循环血糖、食物摄入量、肝脏糖原水平或腹部脂肪垫质量。对肌肉线粒体生物能学的检查显示超氧化物率没有变化。${哦}_2^{\bullet -}$)/过氧化氢 (H ₂ O ₂ ) 或 O ₂在不同呼吸状态下的消耗或脂质过氧化加合物水平的改变，而与小鼠品系或饮食无关。此外，我们测量了从肝组织中分离出的线粒体的生物能学，发现 GRX2 的部分缺失增强了呼吸作用，但并未改变 ROS 的产生。

讨论：总体而言，我们的研究结果表明，在保护雌性 GRX2+/- 小鼠免受 DIO、脂肪堆积、肝内脂质积累以及来自肌肉和肝脏组织的线粒体生物能学方面存在性别差异。