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碧萝芷对成熟 3T3-L1 脂肪细胞葡萄糖转运的影响。

Effect of pycnogenol on glucose transport in mature 3T3-L1 adipocytes.

机构信息

Department of Biomedical Science, CHA University, Seongnam, Gyeonggi 463-836, Korea.

出版信息

Phytother Res. 2010 Aug;24(8):1242-9. doi: 10.1002/ptr.3193.

DOI:10.1002/ptr.3193
PMID:20658573
Abstract

Pycnogenol, a procyanidins-enriched extract of Pinus maritima bark, possesses antidiabetic properties, which improves the altered parameters of glucose metabolism that are associated with type 2 diabetes mellitus (T2DM). Since the insulin-stimulated antidiabetic activities of natural bioactive compounds are mediated by GLUT4 via the phosphatidylinositol-3-kinase (PI3K) and/or p38 mitogen activated protein kinase (p38-MAPK) pathway, the effects of pycnogenol were examined on the molecular mechanism of glucose uptake by the glucose transport system. 3T3-L1 adipocytes were treated with various concentrations of pycnogenol, and glucose uptake was examined using a non-radioisotope enzymatic assay and by molecular events associated with the glucose transport system using semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). The results show that pycnogenol increased glucose uptake in fully differentiated 3T3-L1 adipocytes and increased the relative abundance of both GLUT4 and Akt mRNAs through the PI3K pathway in a dose dependent manner. Furthermore, pycnogenol restored the PI3K antagonist-induced inhibition of glucose uptake in the presence of wartmannin, an inhibitor of the PI3K. Overall, these results indicate that pycnogenol may stimulate glucose uptake via the PI3K dependent tyrosine kinase pathways involving Akt. Further the results suggest that pycnogenol might be useful in maintaining blood glucose control.

摘要

碧萝芷,一种富含原花青素的法国海岸松树皮提取物,具有抗糖尿病特性,可改善与 2 型糖尿病(T2DM)相关的葡萄糖代谢改变参数。由于天然生物活性化合物的胰岛素刺激抗糖尿病活性是通过葡萄糖转运系统中的 GLUT4 介导的,通过磷脂酰肌醇-3-激酶(PI3K)和/或 p38 有丝分裂原激活蛋白激酶(p38-MAPK)途径,研究了碧萝芷对葡萄糖摄取分子机制的影响。用不同浓度的碧萝芷处理 3T3-L1 脂肪细胞,并使用非放射性同位素酶测定法和与葡萄糖转运系统相关的分子事件通过半定量逆转录-聚合酶链反应(RT-PCR)来检查葡萄糖摄取。结果表明,碧萝芷增加了完全分化的 3T3-L1 脂肪细胞中的葡萄糖摄取,并通过 PI3K 途径以剂量依赖性方式增加了 GLUT4 和 Akt mRNA 的相对丰度。此外,碧萝芷在 wortmannin(PI3K 的抑制剂)存在下恢复了 PI3K 拮抗剂诱导的葡萄糖摄取抑制。总体而言,这些结果表明碧萝芷可能通过涉及 Akt 的 PI3K 依赖性酪氨酸激酶途径刺激葡萄糖摄取。此外,结果表明碧萝芷可能有助于维持血糖控制。

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