阿卡波糖可降低蔗糖诱导高血压大鼠的血压。

Israel journal of medical sciences Pub Date : 1997-03-01
Z Madar, E C Melamed, R Zimlichman
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引用次数: 0

摘要

高血压通常与糖耐量受损和胰岛素水平升高有关,这些因素会导致胰岛素抵抗。本研究评估了阿卡波糖的作用,阿卡波糖是一种抑制蔗糖诱导的高血压大鼠碳水化合物消化的降糖药物。在16周的时间里,研究了3组大鼠饲粮的影响:蔗糖+ NaCl(1%湿体积[w/v])加阿卡波糖(0.04%湿重[w/w]),蔗糖+ NaCl (1% w/v)不加阿卡波糖,第三组为复合碳水化合物。喂食或不喂食阿卡波糖的大鼠体重无统计学差异。用阿卡波糖治疗时,空腹血糖水平显著降低。喂食蔗糖+阿卡波糖的大鼠餐后血糖和胰岛素水平降低。蔗糖+ NaCl喂养3个月的大鼠收缩压显著升高(p < 0.001),而糖喂养的大鼠收缩压维持在初始水平。喂食复合碳水化合物组的血压变化低于喂食蔗糖的大鼠。与不加糖组相比,加糖组大鼠尿量、Na+、K+均有增加的趋势(p < 0.05)。我们得出结论,高胰岛素水平、糖耐量受损和Na+潴留可能导致蔗糖诱导的高血压的发生。阿卡波糖可防止蔗糖引起的血浆葡萄糖和胰岛素水平升高。尿钠离子的增加可能间接促成这种作用,从而导致正常的收缩压。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Acarbose reduces blood pressure in sucrose-induced hypertension in rats.

Hypertension is often associated with impaired glucose tolerance and high insulin levels, factors that contribute to insulin resistance. The present study evaluates the effect of acarbose, a hypoglycemic drug that inhibits carbohydrate digestion in sucrose-induced hypertension in rats. The effects of diets fed to 3 groups of rats for a 16-week period were studied: sucrose + NaCl (1% wet volume [w/v]) with acarbose (0.04% wet weight [w/w]), sucrose + NaCl (1% w/v) without acarbose, and a third diet of complex carbohydrates. There was no statistical difference in the body weight between rats fed with or without acarbose. Fasting glucose levels were significantly lowered when treated with acarbose. Postprandial blood glucose and insulin levels were attenuated in rats fed sucrose + acarbose. Systolic blood pressure increased significantly (p < 0.001) in rats fed sucrose + NaCl for 3 months, whereas systolic blood pressure of acarbose-fed rats remained at the initial level. Blood pressure changes in the complex carbohydrate-fed group were lower than in rats fed sucrose. The urinary volume, Na+, and K+ of rats fed acarbose tended to increase compared to the acarbose-free diet (p < 0.05). We conclude that high insulin levels, impaired glucose tolerance and Na+ retention may contribute to the development of sucrose-induced hypertension. Acarbose prevents sucrose-induced increases in plasma glucose and insulin levels. Increases in urinary Na + may contribute indirectly to this effect with resultant normal systolic blood pressures.

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