Department of Clinical Korean Medicine, Graduate School, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea.
Int J Mol Sci. 2019 Feb 8;20(3):727. doi: 10.3390/ijms20030727.
Insulin resistance is strongly associated with the metabolic syndrome, and chronic inflammation is known to be a major mechanism of insulin resistance and is a therapeutic target. This study was designed to evaluate the effect of (SB) in high-fat diet (HFD)-induced insulin-resistant mice and to investigate its mechanism based on inflammatory responses. Mice were fed a HFD to induce insulin resistance and then administered SB for nine weeks. Body weight, glucose, lipid, insulin, epididymal fat pad and liver weights, and histologic characteristics were evaluated to determine the effect on insulin resistance. In order to evaluate the effects on the inflammatory process, we analyzed the proportions of macrophages in liver and epididymal fat and measured inflammatory gene expression. Fasting and postprandial glucose, fasting insulin, HOMA-IR, triglycerides, and low density lipoprotein cholesterol levels were significantly decreased by SB administration. The epididymal fat and liver showed significant weight decreases and histological improvements. Total adipose tissue macrophages (ATMs) decreased (27.71 ± 3.47% vs. 45.26 ± 7.26%, < 0.05), M2 ATMs increased (47.02 ± 6.63% vs. 24.28 ± 8.00%, < 0.05), and CD11b⁺ Kupffer cells decreased. The expression levels of tumor necrosis factor alpha and F4/80 in the liver were significantly decreased (12.03 ± 1.47% vs. 25.88 ± 4.57%, < 0.05) compared to HFD group. These results suggest that SB improved insulin resistance through inhibition of macrophage-mediated inflammation.
胰岛素抵抗与代谢综合征密切相关，慢性炎症是胰岛素抵抗的主要机制之一，也是治疗的靶点。本研究旨在评估 SB 对高脂肪饮食（HFD）诱导的胰岛素抵抗小鼠的作用，并基于炎症反应探讨其机制。将小鼠喂食 HFD 以诱导胰岛素抵抗，然后给予 SB 治疗 9 周。评估胰岛素抵抗的指标包括体重、血糖、血脂、胰岛素、附睾脂肪垫和肝脏重量以及组织学特征。为了评估对炎症过程的影响，我们分析了肝脏和附睾脂肪中巨噬细胞的比例，并测量了炎症基因的表达。SB 给药可显著降低空腹和餐后血糖、空腹胰岛素、HOMA-IR、甘油三酯和低密度脂蛋白胆固醇水平。附睾脂肪和肝脏重量明显减轻，组织学改善。总脂肪组织巨噬细胞（ATMs）减少（27.71±3.47%比 45.26±7.26%， < 0.05），M2 ATMs 增加（47.02±6.63%比 24.28±8.00%， < 0.05），CD11b⁺Kupffer 细胞减少。与 HFD 组相比，肝脏中肿瘤坏死因子 α 和 F4/80 的表达水平显著降低（12.03±1.47%比 25.88±4.57%， < 0.05）。这些结果表明，SB 通过抑制巨噬细胞介导的炎症改善胰岛素抵抗。
