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没食子酸表没食子儿茶素酯可延缓自发性非肥胖型糖尿病小鼠 1 型糖尿病的发病。

Epigallocatechin gallate delays the onset of type 1 diabetes in spontaneous non-obese diabetic mice.

机构信息

Department of Human Nutrition, Foods and Exercise, College of Agriculture and Life Sciences, Virginia Polytechnic Institute and State University, 1880 Pratt Drive, Corporate Research Center, Blacksburg, VA 24060, USA.

出版信息

Br J Nutr. 2011 Apr;105(8):1218-25. doi: 10.1017/S0007114510004824. Epub 2010 Dec 9.

DOI:10.1017/S0007114510004824
PMID:21144096
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4335671/
Abstract

Type 1 diabetes (T1D) results from the autoimmune-mediated destruction of pancreatic β-cells, leading to deficiency of insulin production. Successful islet transplantation can normalise hyperglycaemia in T1D patients; however, the limited availability of the islets, loss of islet cell mass through apoptosis after islet isolation and potential autoimmune destruction of the transplanted islets prevent the widespread use of this procedure. Therefore, the search for novel and cost-effective agents that can prevent or treat T1D is extremely important to decrease the burden of morbidity from this disease. In the present study, we discovered that ( - )-epigallocatechin gallate (EGCG, 0·05 % in drinking-water), the primary polyphenolic component in green tea, effectively delayed the onset of T1D in non-obese diabetic (NOD) mice. At 32 weeks of age, eight (66·7 %) out of twelve mice in the control group developed diabetes, whereas only three (25 %) out of twelve mice in the EGCG-treated group became diabetic (P < 0·05). Consistently, mice supplemented with EGCG had significantly higher plasma insulin levels and survival rate but lower glycosylated Hb concentrations compared with the control animals. EGCG had no significant effects on food or water intake and body weight in mice, suggesting that the glucose-lowering effect was not due to an alteration in these parameters. While EGCG did not modulate insulitis, it elevated the circulating anti-inflammatory cytokine IL-10 level in NOD mice. These findings demonstrate that EGCG may be a novel, plant-derived compound capable of reducing the risk of T1D.

摘要

1 型糖尿病(T1D)是由胰腺β细胞的自身免疫介导破坏引起的,导致胰岛素产生不足。胰岛成功移植可以使 T1D 患者的高血糖正常化;然而,胰岛的有限可用性、胰岛分离后通过细胞凋亡导致的胰岛细胞质量损失以及移植胰岛的潜在自身免疫破坏,阻止了该程序的广泛应用。因此,寻找新的、具有成本效益的药物来预防或治疗 T1D 非常重要,可以降低这种疾病的发病率。在本研究中,我们发现(-)-表没食子儿茶素没食子酸酯(EGCG,饮用水中 0·05%),绿茶中的主要多酚成分,可有效延缓非肥胖型糖尿病(NOD)小鼠 T1D 的发病。在 32 周龄时,对照组的 12 只小鼠中有 8 只(66·7%)发生糖尿病,而 EGCG 治疗组的 12 只小鼠中只有 3 只(25%)发生糖尿病(P<0·05)。一致地,与对照组动物相比,补充 EGCG 的小鼠具有更高的血浆胰岛素水平和生存率,但糖化血红蛋白浓度更低。EGCG 对小鼠的食物或水摄入量和体重没有显著影响,这表明其降血糖作用不是由于这些参数的改变。虽然 EGCG 没有调节胰岛炎,但它提高了 NOD 小鼠的循环抗炎细胞因子 IL-10 水平。这些发现表明,EGCG 可能是一种新型的植物来源化合物,能够降低 T1D 的发病风险。

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Flavonoids have differential effects on glucose absorption in rats (Rattus norvegicus) and American robins (Turdis migratorius).类黄酮对大鼠(Norvegicus 大鼠)和美洲知更鸟(Turdis migratorius)的葡萄糖吸收有不同的影响。
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