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球蛋白消化产物及其活性成分 Leu-Ser-Glu-Leu 对 ICR 小鼠、链脲佐菌素诱导的糖尿病小鼠和 KK-Ay 小鼠的降血糖作用。

Anti-diabetic effects of globin digest and its active ingredient Leu-Ser-Glu-Leu in ICR mice, streptozotocin-induced diabetic mice and KK-Ay mice.

机构信息

MG Pharma Inc, 7-7-25 Saito-Asagi, Ibaraki, Osaka 567-0085, Japan.

出版信息

Life Sci. 2010 Mar 13;86(11-12):424-34. doi: 10.1016/j.lfs.2010.01.014. Epub 2010 Jan 25.

Abstract

AIMS

Leu-Ser-Glu-Leu (LSEL) is the main active ingredient of globin digest (GD) that has an anti-diabetic effect. Here, we investigated the anti-diabetic effect of LSEL for the first time.

MAIN METHODS

The anti-diabetic effects of GD and LSEL in ICR mice, streptozotocin (STZ)-induced diabetic mice and KK-Ay mice were examined.

KEY FINDINGS

GD and LSEL suppressed the elevation of blood glucose in an oral glucose tolerance test (OGTT) in ICR mice, STZ-induced diabetic mice and KK-Ay mice as well as in an oral sucrose tolerance test in ICR mice and in an insulin tolerance test (ITT) in KK-Ay mice. GD and LSEL decreased the blood glucose levels in the basal state in STZ-induced diabetic mice and KK-Ay mice. Furthermore, GD and LSEL elevated the serum insulin levels in an OGTT in ICR mice and KK-Ay mice and promoted the use of insulin in an ITT in KK-Ay mice. GD and LSEL increased the translocation or expression of the glucose transporter 4 in the muscle of ICR mice, STZ-induced diabetic mice and KK-Ay mice and increased the expression of the uncoupling protein 2 (UCP2) in the muscle of ICR mice.

SIGNIFICANCE

These results indicate that GD and LSEL control blood glucose through the promotion of glucose uptake in the muscle of the mice. The acceleration of glucose uptake by GD and LSEL may be controlled by the promotion of insulin secretion and the up-regulation of UCP2 expression. GD and LSEL seem to be useful for lowering the incidence of hyperglycemia.

摘要

目的

Leu-Ser-Glu-Leu(LSEL)是球蛋白消化物(GD)的主要活性成分,具有抗糖尿病作用。在这里,我们首次研究了 LSEL 的抗糖尿病作用。

主要方法

在 ICR 小鼠、链脲佐菌素(STZ)诱导的糖尿病小鼠和 KK-Ay 小鼠中检查了 GD 和 LSEL 的抗糖尿病作用。

主要发现

GD 和 LSEL 抑制了 ICR 小鼠、STZ 诱导的糖尿病小鼠和 KK-Ay 小鼠口服葡萄糖耐量试验(OGTT)中血糖的升高,以及 ICR 小鼠口服蔗糖耐量试验和 KK-Ay 小鼠胰岛素耐量试验(ITT)中血糖的升高。GD 和 LSEL 降低了 STZ 诱导的糖尿病小鼠和 KK-Ay 小鼠基础状态下的血糖水平。此外,GD 和 LSEL 在 OGTT 中提高了血清胰岛素水平在 ICR 小鼠和 KK-Ay 小鼠中,促进了 ITT 中 KK-Ay 小鼠胰岛素的利用。GD 和 LSEL 增加了 ICR 小鼠、STZ 诱导的糖尿病小鼠和 KK-Ay 小鼠肌肉中葡萄糖转运蛋白 4 的易位或表达,并增加了 ICR 小鼠肌肉中解偶联蛋白 2(UCP2)的表达。

意义

这些结果表明,GD 和 LSEL 通过促进小鼠肌肉中的葡萄糖摄取来控制血糖。GD 和 LSEL 加速葡萄糖摄取可能受到促进胰岛素分泌和上调 UCP2 表达的控制。GD 和 LSEL 似乎可用于降低高血糖的发生率。

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