喵ID:ZkqAoB

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

基本信息

DOI:
10.1017/s0007114510004824
10.1017/s0007114510004824
发表时间:
2011-04
2011-04
影响因子:
3.6
3.6
通讯作者:
Liu, Dongmin
Liu, Dongmin
中科院分区:
医学3区
医学3区
文献类型:
Journal Article
Journal Article
作者: Fu, Zhuo;Zhen, Wei;Yuskavage, Julia;Liu, Dongmin
研究方向: Nutrition & Dietetics
MeSH主题词: --
来源链接:pubmed详情页地址

文献摘要

Type 1 diabetes (T1D) results from the autoimmune-mediated destruction of pancreatic b-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.
1型糖尿病(T1D)是由自身免疫介导的胰腺β细胞破坏所致,导致胰岛素产生不足。成功的胰岛移植可使1型糖尿病患者的高血糖恢复正常;然而,胰岛来源有限,胰岛分离后通过细胞凋亡导致胰岛细胞量减少以及移植胰岛可能遭受自身免疫破坏,这些都阻碍了这一方法的广泛应用。因此,寻找能够预防或治疗1型糖尿病的新型且具有成本效益的药物对于减轻该疾病的发病负担极其重要。在本研究中,我们发现(-)-表没食子儿茶素没食子酸酯(EGCG,饮用水中含量为0.05%),即绿茶中的主要多酚成分,可有效延缓非肥胖糖尿病(NOD)小鼠1型糖尿病的发病。在32周龄时,对照组12只小鼠中有8只(66.7%)患糖尿病,而EGCG治疗组12只小鼠中只有3只(25%)患糖尿病(P<0.05)。一致的是,与对照动物相比,补充EGCG的小鼠血浆胰岛素水平显著更高,存活率更高,但糖化血红蛋白浓度更低。EGCG对小鼠的食物或水摄入量以及体重没有显著影响,这表明其降糖作用并非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小鼠体内循环的抗炎细胞因子IL - 10水平。这些发现表明EGCG可能是一种新型的植物源性化合物,能够降低1型糖尿病的风险。
参考文献(64)
被引文献(83)

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数据更新时间:2024-06-01

关联基金

Genistein and cAMP signaling in vascular endothelium
批准号:
7491164
7491164
批准年份:
2007
2007
资助金额:
23.47
23.47
项目类别: