4.4 Article

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

期刊

BRITISH JOURNAL OF NUTRITION
卷 105, 期 8, 页码 1218-1225

出版社

CAMBRIDGE UNIV PRESS
DOI: 10.1017/S0007114510004824

关键词

Type 1 diabetes; Epigallocatechin gallate; Non-obese diabetic mice; Human islets

资金

  1. American Diabetes Association
  2. Virginia Commonwealth Health Research Board
  3. National Institutes of Health [1R21AT004694]

向作者/读者索取更多资源

Type 1 diabetes (T1D) results from the autoimmune-mediated destruction of pancreatic beta-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.

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