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膳食椰子仁蛋白可有益地调节链脲佐菌素诱导的糖尿病大鼠 NFκB 和 RAGE 的表达。

Dietary coconut kernel protein beneficially modulates NFκB and RAGE expression in streptozotocin induced diabetes in rats.

机构信息

Department of Biochemistry, University of Kerala, Kariavattom Campus, Thiruvananthapuram, Kerala 695 581 India ; Department of Biochemistry, Mar Baselios Dental College, Thankalam, Kothamangalam, Eranakulam, Kerala 686 691 India.

Department of Biochemistry, University of Kerala, Kariavattom Campus, Thiruvananthapuram, Kerala 695 581 India.

出版信息

J Food Sci Technol. 2014 Sep;51(9):2141-7. doi: 10.1007/s13197-012-0729-5. Epub 2012 May 11.

Abstract

Previous studies showed that arginine rich coconut kernel protein (CKP) maintains glucose homeostasis in experimental diabetic rats. But the mechanism of this effect was not clear. This study investigated the effect of CKP on the expression of liver receptor for advance glycated end products (RAGE), inducible nitric oxide synthase (iNOS) and NFkB. Diabetes was induced by injecting a single dose of streptozotocin (75 mg/kg body weight) intraperitoneally. After inducing diabetes, CKP was administered to rats orally for 45 days. After the experimental period, serum glucose, insulin, liver glycogen, glucose metabolizing enzyme activities and the expression of liver RAGE, iNOS and NFkB was evaluated. The results showed that CKP beneficially modulated the levels of glucose and insulin as well as the metabolizing enzyme activities. Expression of RAGE and NFkB was found to be over expressed in diabetic rats but was found to be down regulated in CKP fed diabetic rats. iNOS expression was down regulated in diabetic rats, which was expressed normally in CKP fed diabetic rats. These results clearly demonstrated that anti diabetic activity of CKP is mediated through NFkB pathway.

摘要

先前的研究表明,富含精氨酸的椰子仁蛋白(CKP)可维持实验性糖尿病大鼠的葡萄糖内稳态。但这种作用的机制尚不清楚。本研究探讨了 CKP 对肝糖基化终产物受体(RAGE)、诱导型一氧化氮合酶(iNOS)和 NFkB 表达的影响。糖尿病通过腹腔内注射单次剂量链脲佐菌素(75mg/kg 体重)诱导。诱导糖尿病后,CKP 经口给予大鼠 45 天。实验期结束后,评估血清葡萄糖、胰岛素、肝糖原、糖代谢酶活性以及肝 RAGE、iNOS 和 NFkB 的表达。结果表明,CKP 可有益地调节血糖和胰岛素水平以及代谢酶活性。在糖尿病大鼠中发现 RAGE 和 NFkB 的表达过度表达,但在 CKP 喂养的糖尿病大鼠中发现其表达下调。糖尿病大鼠中 iNOS 的表达下调,而 CKP 喂养的糖尿病大鼠中 iNOS 的表达正常。这些结果清楚地表明,CKP 的抗糖尿病活性是通过 NFkB 途径介导的。

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