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柠檬酸可抑制链脲佐菌素(1 型)糖尿病大鼠白内障、蛋白尿和酮症的发展。

Citric acid inhibits development of cataracts, proteinuria and ketosis in streptozotocin (type 1) diabetic rats.

机构信息

Department of Food and Nutrition, Laboratory of Biochemistry & Nutritional Science, Japan Women's University, Bunkyo-ku, Tokyo 112-8681, Japan.

出版信息

Biochem Biophys Res Commun. 2010 Feb 26;393(1):118-22. doi: 10.1016/j.bbrc.2010.01.095. Epub 2010 Feb 1.

Abstract

Although many fruits such as lemon and orange contain citric acid, little is known about beneficial effects of citric acid on health. Here we measured the effect of citric acid on the pathogenesis of diabetic complications in streptozotocin-induced diabetic rats. Although oral administration of citric acid to diabetic rats did not affect blood glucose concentration, it delayed the development of cataracts, inhibited accumulation of advanced glycation end-products (AGEs) such as N(epsilon)-(carboxyethyl)lysine (CEL) and N(epsilon)-(carboxymethyl)lysine (CML) in lens proteins, and protected against albuminuria and ketosis. We also show that incubation of protein with acetol, a metabolite formed from acetone by acetone monooxygenase, generate CEL, suggesting that inhibition of ketosis by citric acid may lead to the decrease in CEL in lens proteins. These results demonstrate that the oral administration of citric acid ameliorates ketosis and protects against the development of diabetic complications in an animal model of type 1 diabetes.

摘要

虽然柠檬和橙子等许多水果都含有柠檬酸,但人们对柠檬酸对健康的有益影响知之甚少。在这里,我们测量了柠檬酸对链脲佐菌素诱导的糖尿病大鼠糖尿病并发症发病机制的影响。虽然柠檬酸的口服给药并不影响糖尿病大鼠的血糖浓度,但它延迟了白内障的发展,抑制了晶状体蛋白中晚期糖基化终产物(AGEs)如 N(ε)-(羧乙基)赖氨酸(CEL)和 N(ε)-(羧甲基)赖氨酸(CML)的积累,并防止了白蛋白尿和酮症。我们还表明,蛋白质与丙酮单加氧酶由丙酮形成的代谢物乙酰醇孵育会产生 CEL,这表明柠檬酸抑制酮症可能导致晶状体蛋白中 CEL 的减少。这些结果表明,柠檬酸的口服给药可改善酮症并防止 1 型糖尿病动物模型中糖尿病并发症的发展。

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