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支链氨基酸补充剂可保护链脲佐菌素诱导的胰岛素分泌及其相关机制。

Branched-chain amino acids supplementation protects streptozotocin-induced insulin secretion and the correlated mechanism.

机构信息

Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China.

出版信息

Biofactors. 2015 Mar-Apr;41(2):127-33. doi: 10.1002/biof.1188. Epub 2014 Oct 30.

DOI:10.1002/biof.1188
PMID:25359484
Abstract

Significant evidence demonstrates that oxidative stress can impair insulin secretion and contribute to the development of type 2 diabetes. Branched-chain amino acids (BCAAs) are reported to be positively related to insulin secretion. This study aimed to determine how oxidative stress affects the function of islets and whether BCAAs can ameliorate the oxidative stress, and accompanying c-jun N-terminal kinase (JNK), protein kinase D1 (PKD1), and pancreatic/duodenal homeobox-1 (PDX-1) changes induced by streptozotocin (STZ). Plasma glucose, plasma insulin, and JNK, PKD1 and PDX-1 mRNA and protein expression were measured in rats treated with STZ and BCAAs. The glucose level in STZ-induced diabetic rats was much higher than that in control animals, and the elevated plasma glucose level in diabetic rats could be significantly inhibited by BCAAs treatment. Consistent with the change in glucose levels, the levels of insulin were also affected by BCAAs treatment. The mRNA and protein expression of JNK, PDX-1, and PKD1 were significantly altered in diabetic rats compared with the control group (P<0.01) and treatment with a low dose of BCAA reversed these changes in those above markers significantly (P<0.01). The present study demonstrated that STZ-induced oxidative stress could reduce serum insulin levels and alter the JNK, PDX-1, and PKD1 expression. BCAAs restored the levels of serum insulin reversed changes in JNK, PDX-1, and PKD1 expression.

摘要

大量证据表明,氧化应激会损害胰岛素分泌,并导致 2 型糖尿病的发生。支链氨基酸(BCAAs)被报道与胰岛素分泌呈正相关。本研究旨在确定氧化应激如何影响胰岛的功能,以及支链氨基酸是否可以改善氧化应激以及随之而来的 c-jun N 末端激酶(JNK)、蛋白激酶 D1(PKD1)和胰腺/十二指肠同源盒-1(PDX-1)变化由链脲佐菌素(STZ)诱导。用 STZ 和 BCAAs 处理大鼠后,测量血浆葡萄糖、血浆胰岛素以及 JNK、PKD1 和 PDX-1 mRNA 和蛋白表达。STZ 诱导的糖尿病大鼠的血糖水平明显高于对照组,而糖尿病大鼠的升高血糖水平可以通过 BCAAs 治疗得到显著抑制。与血糖水平的变化一致,胰岛素水平也受到 BCAAs 治疗的影响。与对照组相比,JNK、PDX-1 和 PKD1 的 mRNA 和蛋白表达在糖尿病大鼠中明显改变(P<0.01),而低剂量 BCAAs 治疗显著逆转了这些标志物的变化(P<0.01)。本研究表明,STZ 诱导的氧化应激可降低血清胰岛素水平,并改变 JNK、PDX-1 和 PKD1 的表达。BCAAs 恢复了血清胰岛素水平,逆转了 JNK、PDX-1 和 PKD1 表达的变化。

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