冰岛刺参岩藻糖基化硫酸软骨素降血糖及改善胰岛素抵抗的研究

Study of fucosylated chondroitin sulfate from Cucumaria frondosa on hyperglycemic effects and insulin resistance improvement

以高脂高糖饲料(high-fat high-sucrose,HFSD)饲喂法建立胰岛素抵抗小鼠模型。研究了冰岛刺参岩藻糖基化硫酸软骨素(fucosylated chondroitin sulfate from the sea cucumber Cucumaria frondosa,Cf-CHS)对胰岛素抵抗小鼠的降血糖及改善胰岛素抵抗作用。雄性C57BL/6J小鼠随机分为正常对照(标准饲料)、模型对照(HFSD)、阳性对照(HFSD+rosiglitazone(RSG),1mg·(kg·d)-1)、Cf-CHS组(HFSD+Cf-CHS,80mg·(kg·d)-1)及Cf-CHS+RSG组(HFSD+Cf-CHS+RSG,80+1mg·(kg·d)-1)。各组小鼠自由摄食摄水19周。实验结束后,称重小鼠白色脂肪质量,检测空腹血糖、血清胰岛素及血清脂联素、抵抗素、瘦素、肿瘤坏死因子-α(TNF-α)水平。实验结果表明:Cf-CHS可显著降低胰岛素抵抗小鼠的脂肪积累(p<0.01),降低血糖(p<0.01)和胰岛素(p<0.05)水平,改善胰岛素抵抗(p<0.05),提高血清脂联素含量(p<0.05),降低抵抗素(p<0.01)、瘦素(p<0.01)和TNF-α(p<0.05)含量。Cf-CHS与RSG复配使用,效果更显著(p<0.05,p<0.01)。Cf-CHS能显著改善胰岛素抵抗小鼠的高血糖症状及胰岛素抵抗程度,其作用机制可能与改善肥胖引起的脂肪细胞因子的分泌紊乱有关。

The model mice was established by feeding a diet of high-fat high-sucrose diet（ HFSD）.The aim of the present study was to unravel the effects of fucosylated chondroitin sulfate from Cucumaria frondosa （Cf-CHS）on hyperglycemic effects and insulin resistance improvement in insulin resistant mice. Male C57BL/6 mice were randomly assigned into the normal control （ standard diet）, model control （ HFSD）, positive control （ HFSD ＋ rosiglitazone（RSG）, 1mg. （ kg· d） -1 ）, Cf- CHS （ HFSD ＋ ＋ Cf- CHS, 8Omg. （ kg. d） -1 ）, Cf- CHS ＋ RSG （ HFSD ＋ Cf -CHS ＋ RSG, 80 ＋ 1mg · （kg·d） -1） groups. All animals fed with diet and water freely for 19 weeks. After experiments,the white fat weight, fasting serum glucose, serum insulin, serum adiponectin, resistin, leptin, and tumor necrosis factor-a （TNF-α）levels were determined. Results showed that Cf-CHS markedly decreased fat deposition （ p 〈 0.01 ）, blood sugar （ p 〈 0.01 ） and insulin （ p 〈 0.0.5 ） levels, ameliorated insulin resistance （ p 〈 0.05 ）, increased serum adiponectin concentration （ p 〈 0.05 ）, and lowered serum resistin （ p 〈 0.01 ）, leptin （ p 〈 0.01 ）, TNF-α（p 〈 0.05）levels.The effect was more significant when Cf- CHS compounded with RSG （ p 〈 0.05,P 〈 0.01 ）. Cf-CHS significantly decreased blood glucose level and ameliorated insulin resistance in insulin resistant mice, and the mechanisms may involved the regulation of adipocytokines parasecretion caused by adiposity.