Department of Public Health, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Department of Public Health, Faculty of Medicine, Universitas Padjadjaran, Bandung, Indonesia.
Biol Trace Elem Res. 2018 Jan;181(1):71-81. doi: 10.1007/s12011-017-1013-3. Epub 2017 Apr 20.
Oxidative stress in obesity leads to insulin resistance in type 2 diabetes. Some selenoproteins possess antioxidant properties, suggesting that selenium (Se) may protect against type 2 diabetes; however, evidence from epidemiological studies is contradictory. We hypothesized that Se status before supplementation (baseline) contributes to the supplementation outcome. This study aimed to clarify the influence of baseline Se status on the effect of Se supplementation on the diabetic condition. Six-week-old KKAy mice were fed a diet without supplemental Se or with 0.1 ppm Se in the form of L-selenomethionine (SeM) for 2 weeks to create low-Se and sufficient-Se baseline statuses, respectively. For the next 4 weeks, low-Se mice were given a SeM (0.5 ppm Se)-supplemented diet, and sufficient-Se mice were given either a SeM (0.5 ppm Se)- or sodium selenite (0.5 ppm Se)-supplemented diet; control groups continued on baseline diets. Serum Se concentrations, glutathione peroxidase (GPx) activities, adiponectin levels, glucose tolerance, and insulin sensitivity were analyzed. All mice became diabetic during the 2-week baseline induction period. At the end of the supplementation period, Se-receiving groups demonstrated significantly higher Se concentrations and GPx activities than their respective controls. Sufficient-Se mice receiving SeM had lower blood glucose levels and better insulin sensitivity than control and sodium selenite-receiving mice, whereas low-Se mice receiving SeM showed no such improvements compared with their controls. Our results suggest that Se supplementation in the form of SeM may help prevent type 2 diabetes aggravation in people taking the 55 μg/day Se recommended dietary allowance.
肥胖中的氧化应激导致 2 型糖尿病中的胰岛素抵抗。一些硒蛋白具有抗氧化特性,这表明硒(Se)可能对 2 型糖尿病有保护作用;然而,来自流行病学研究的证据存在矛盾。我们假设补充前的 Se 状态(基线)会影响补充的结果。本研究旨在阐明基线 Se 状态对 Se 补充对糖尿病状况影响的作用。将 6 周龄的 KKAy 小鼠分别用不含补充 Se 的饮食或含 0.1ppm L-硒蛋氨酸(SeM)的饮食喂养 2 周,以分别建立低 Se 和充足 Se 的基线状态。在接下来的 4 周内,低 Se 组给予补充 SeM(0.5ppm Se)的饮食,而充足 Se 组给予补充 SeM(0.5ppm Se)或亚硒酸钠(0.5ppm Se)的饮食;对照组继续给予基础饮食。分析血清 Se 浓度、谷胱甘肽过氧化物酶(GPx)活性、脂联素水平、葡萄糖耐量和胰岛素敏感性。所有小鼠在 2 周的基线诱导期内都发生了糖尿病。在补充期结束时,接受 Se 的各组的 Se 浓度和 GPx 活性明显高于各自的对照组。接受 SeM 的充足 Se 小鼠的血糖水平较低,胰岛素敏感性较好,优于接受亚硒酸钠的对照组和接受 SeM 的对照组,而接受 SeM 的低 Se 小鼠与对照组相比则没有改善。我们的结果表明,以 SeM 的形式补充 Se 可能有助于预防每天推荐膳食允许量 55μg 的 Se 摄入的人群中 2 型糖尿病的恶化。