Biomedical Institute, Research Center, Hayashibara Biochemical Laboratories, Inc., 675-1 Fujisaki, Okayama 702-8006, Japan.
Nutr Res. 2010 Dec;30(12):840-8. doi: 10.1016/j.nutres.2010.10.009.
Trehalose has been shown to evoke lower insulin secretion than glucose in oral saccharide tolerance tests in humans. Given this hypoinsulinemic effect of trehalose, we hypothesized that trehalose suppresses adipocyte hypertrophy by reducing storage of triglyceride and mitigates insulin resistance in mice fed a high-fat diet (HFD). Mice were fed an HFD and given drinking water containing 2.5% saccharide (glucose [Glc], trehalose [Tre], maltose [Mal], high-fructose corn syrup, or fructose [Fru]) ad libitum. After 7 weeks of HFD and saccharide intake, fasting serum insulin levels in the Tre/HFD group were significantly lower than in the Mal/HFD and Glc/HFD groups (P < .05). Furthermore, the Tre/HFD group showed a significantly suppressed elevation of homeostasis model assessment-insulin resistance compared with the Mal/HFD group (P < .05) and showed a trend toward lower homeostasis model assessment-insulin resistance than the Glc/HFD group. After 8 weeks of feeding, mesenteric adipocyte size in the Tre/HFD group showed significantly less hypertrophy than the Glc/HFD, Mal/HFD, high-fructose corn syrup/HFD, or Fru/HFD group. Analysis of gene expression in mesenteric adipocytes showed that no statistically significant difference in the expression of monocyte chemoattractant protein-1 (MCP-1) messenger RNA (mRNA) was observed between the Tre/HFD group and the distilled water/standard diet group, whereas a significant increase in the MCP-1 mRNA expression was observed in the Glc/HFD, Mal/HFD, Fru/HFD, and distilled water/HFD groups. Thus, our data indicate that trehalose prevents adipocyte hypertrophy and mitigates insulin resistance in HFD-fed mice by reducing insulin secretion and down-regulating mRNA expression of MCP-1. These findings further suggest that trehalose is a functional saccharide that mitigates insulin resistance.
海藻糖在人体口服糖耐受性试验中被证明比葡萄糖引起的胰岛素分泌少。鉴于海藻糖的这种低胰岛素作用，我们假设海藻糖通过减少甘油三酯的储存来抑制脂肪细胞肥大，并减轻高脂肪饮食（HFD）喂养的小鼠的胰岛素抵抗。小鼠喂食 HFD 并自由饮用含有 2.5%糖（葡萄糖[Glc]、海藻糖[Tre]、麦芽糖[Mal]、高果糖玉米糖浆或果糖[Fru]）的水。在 HFD 和糖摄入 7 周后，Tre/HFD 组的空腹血清胰岛素水平明显低于 Mal/HFD 和 Glc/HFD 组（P <.05）。此外，Tre/HFD 组与 Mal/HFD 组相比，稳态模型评估-胰岛素抵抗显著抑制升高（P <.05），并且与 Glc/HFD 组相比，稳态模型评估-胰岛素抵抗呈下降趋势。喂养 8 周后，Tre/HFD 组肠系膜脂肪细胞大小明显小于 Glc/HFD、Mal/HFD、高果糖玉米糖浆/HFD 或 Fru/HFD 组。对肠系膜脂肪细胞基因表达的分析表明，Tre/HFD 组与蒸馏水/标准饮食组之间单核细胞趋化蛋白-1（MCP-1）信使 RNA（mRNA）的表达没有统计学差异，而 Glc/HFD、Mal/HFD、Fru/HFD 和蒸馏水/HFD 组的 MCP-1 mRNA 表达显著增加。因此，我们的数据表明，海藻糖通过减少胰岛素分泌和下调 MCP-1 mRNA 的表达来防止 HFD 喂养的小鼠脂肪细胞肥大并减轻胰岛素抵抗。这些发现进一步表明，海藻糖是一种具有功能性的糖，可减轻胰岛素抵抗。
