Laboratory of Biochemistry, Department of Biomedical Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, Hokkaido 060-0818, Japan.
Laboratory of Biochemistry, Department of Biomedical Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, Hokkaido 060-0818, Japan; Department of Biochemistry, Faculty of Veterinary Medicine, Alexandria University, Behera, 22785, Egypt.
Nutr Res. 2018 Oct;58:17-25. doi: 10.1016/j.nutres.2018.06.012. Epub 2018 Jul 3.
Dietary supplementation with melinjo (Gnetum gnemon L.) seed extract (MSE) has been proposed as an anti-obesity strategy. However, it remains unclear how MSE modulates energy balance. We tested the hypothesis that dietary MSE reduces energy intake and/or increases physical activity and metabolic thermogenesis in brown and white adipose tissue (BAT and WAT) in mice. Twenty-four C57BL/6 J mice were provided with normal diet, high-fat diet (HFD), or HFD with 1% MSE added, for 17 weeks. Food intake, spontaneous locomotor activity, hepatic triglyceride (TG) content, and blood parameters were examined. Mitochondrial thermogenesis-associated molecule and inflammatory marker expression levels in BAT and WAT were examined by quantitative PCR and western blotting. Dietary MSE did not affect energy intake or spontaneous locomotor activity, but significantly suppressed HFD-induced fat accumulation, hyperglycemia, and hyperinsulinemia. Homeostasis model assessment of insulin resistance score and hepatic TG content were both lower in the MSE-supplemented HFD-fed group than in the HFD-fed group, indicating reduced insulin resistance and a less fatty liver. Dietary MSE upregulated thermogenic uncoupling protein 1 (UCP1) and mitochondrial marker cytochrome c oxidase subunit IV protein expression in BAT; this was closely associated with sirtuin 1 mRNA induction. mRNAs of adipose inflammatory markers, such as monocyte chemotactic 1 and interleukin-1, were induced by HFD but suppressed by MSE. Considering that UCP1 protein expression is the most physiologically relevant parameter to assess the thermogenic capacities of BAT, our results indicate that dietary MSE supplementation induces BAT thermogenesis and reduces obesity-associated adipose tissue inflammation, hepatic steatosis, and insulin resistance.
食用木莲（Gnetum gnemon L.）种仁提取物（MSE）已被提议作为一种抗肥胖策略。然而，MSE 如何调节能量平衡仍不清楚。我们检验了这样一个假设，即饮食中的 MSE 可减少能量摄入和/或增加棕色和白色脂肪组织（BAT 和 WAT）中的体力活动和代谢产热。将 24 只 C57BL/6 J 小鼠分别给予正常饮食、高脂肪饮食（HFD）或添加 1% MSE 的 HFD，喂养 17 周。检测食物摄入量、自发运动活性、肝三酰甘油（TG）含量和血液参数。通过定量 PCR 和 Western 印迹检测 BAT 和 WAT 中与线粒体产热相关的分子和炎症标志物的表达水平。饮食中的 MSE 不影响能量摄入或自发运动活性，但可显著抑制 HFD 诱导的脂肪堆积、高血糖和高胰岛素血症。MSE 补充 HFD 喂养组的稳态模型评估的胰岛素抵抗评分和肝 TG 含量均低于 HFD 喂养组，表明胰岛素抵抗降低和脂肪肝减轻。饮食中的 MSE 上调了 BAT 中的解偶联蛋白 1（UCP1）和线粒体标志物细胞色素 c 氧化酶亚基 IV 蛋白的表达；这与 SIRT1 mRNA 的诱导密切相关。HFD 诱导了脂肪炎症标志物如单核细胞趋化蛋白 1 和白细胞介素-1 的 mRNA 表达，但 MSE 抑制了其表达。考虑到 UCP1 蛋白表达是评估 BAT 产热能力最具生理相关性的参数，我们的结果表明，饮食中 MSE 的补充可诱导 BAT 产热，并减少与肥胖相关的脂肪组织炎症、肝脂肪变性和胰岛素抵抗。
