茶多糖和茶多酚的降血糖作用研究

doi:10.13305/j.cnki.jts.2005.03.011

摘要/Abstract

摘要： 目的研究茶多糖、茶多酚对四氧嘧啶致糖尿病SD大鼠的降血糖作用和机制。方法饲喂SD大鼠茶多糖、茶多酚3周后,观察大鼠血糖、葡萄糖耐量、血胰岛素以及小肠糖降解酶（淀粉酶、蔗糖酶、麦芽糖酶）变化。结果茶多糖、茶多酚都有显著抑制糖尿病大鼠血糖升高的作用;与对照组比较,茶多糖组大鼠血胰岛素水平有显著提高（P<0.05）,蔗糖酶和麦芽糖酶活性显著降低（P<0.05）;茶多酚组的血胰岛素水平有升高趋势,小肠各降解酶活力也有下降趋势,但与对照组比较均未达到显著水平。结论茶多糖对高血糖大鼠有显著的抑制血糖升高的作用,茶多糖的作用机制可能是抑制小肠糖降解酶活性。

关键词: 茶多糖, 茶多酚, 糖尿病, 降血糖

Abstract: The investigation on the hypoglycemic mechanism of tea polysaccharides and tea polyphenol in diabetic SD rats induced by alloxan was conducted. Methods: After feeding tea polysaccharides or polyphenols for 3 weeks, the changes of the level of blood glucose, insulin and the activities of amylase, sucrase and maltase in small intestine were inspected in diabetic rats. Results about that the suppressive effect of high level of blood glucose induced by alloxan was observed in the groups feeded with tea polysaccharides or tea polyphenols obviously in the experimental period. Compared with control group, the level of blood insulin in the group feeded with tea polysaccharides was increased significantly (P<0.05), the activity of sucrase and maltase were decreased significantly. Almost the same change without significance was observed in the group feeded with tea polyphenols while compared with the control group. Investigation indicated that the tea polysaccharides and tea polyphenols have remarkable suppressive hyperglycemic effect on diabetic rats induced by alloxan. These results suggested that functionary mechanisms of the suppressive hyperglycemic effect of tea polysaccharides may be induced by controlling the activities of sucrase and maltase.

Key words: Tea polysaccharides, Tea polyphenols, Diabetic mellitus, Hypoglycemic effect

中图分类号:

丁仁凤, 何普明, 揭国良. 茶多糖和茶多酚的降血糖作用研究[J]. 茶叶科学, 2005, 25(3): 219-224. doi: 10.13305/j.cnki.jts.2005.03.011.

DING Ren-feng, HE Pu-ming, JIE Guo-liang. Study on the Hypoglycemic Mechanism of Tea Polysaccharides and Tea Polyphenols[J]. Journal of Tea Science, 2005, 25(3): 219-224. doi: 10.13305/j.cnki.jts.2005.03.011.

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