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2 型糖尿病大鼠模型中胰岛素受体底物 1 与郎格汉斯胰岛的关系。

Relationship Between Insulin-Receptor Substrate 1 and Langerhans' Islet in a Rat Model of Type 2 Diabetes Mellitus.

机构信息

Department of Immunopathology, Mochtar Riady Institute for Nanotechnology, Tangerang, Indonesia;

Department of Anatomy, Faculty of Medicine, Universitas Pelita Harapan, Tangerang, Indonesia.

出版信息

In Vivo. 2021 Jan-Feb;35(1):291-297. doi: 10.21873/invivo.12258.

Abstract

BACKGROUND/AIM: In vivo studies on pathogenesis of type 2 diabetes mellitus (T2DM) have been reported, however, the relationship between insulin-receptor substrate 1 (IRS1) and the area of Langerhans' islets was unknown. Therefore, a correlation between both parameters was assessed.

MATERIALS AND METHODS

Diabetic groups were fed with a high-fat diet (HFD) and injected with three different doses of streptozotocin, namely 25, 35 and 45 mg/kg, and compared to a control group after 9 weeks.

RESULTS

Administration of HFD/streptozotocin increased the level of fasting blood glucose but reduced the level of IRS1 and the area of Langerhans' islets in diabetic groups. The coefficient of correlation between IRS1 and area of Langerhans' islets was 0.259 (p=0.232). In addition, the coefficient of correlation for fasting blood glucose with the area of Langerhans' islets and IRS1 was -0.520 (p=0.011) and -0.603 (p=0.002), respectively.

CONCLUSION

The reduction of IRS1 was weakly correlated with the destruction of Langerhans' islets, suggesting there is an intermediate step between both parameters.

摘要

背景/目的:已经有关于 2 型糖尿病(T2DM)发病机制的体内研究报告,然而,胰岛素受体底物 1(IRS1)与胰岛朗格汉斯区面积之间的关系尚不清楚。因此,评估了这两个参数之间的相关性。

材料和方法

糖尿病组给予高脂肪饮食(HFD)并注射不同剂量的链脲佐菌素(25、35 和 45mg/kg),9 周后与对照组进行比较。

结果

HFD/链脲佐菌素的给药增加了空腹血糖水平,但降低了糖尿病组中 IRS1 和胰岛朗格汉斯区面积的水平。IRS1 与胰岛朗格汉斯区面积之间的相关系数为 0.259(p=0.232)。此外,空腹血糖与胰岛朗格汉斯区面积和 IRS1 的相关系数分别为-0.520(p=0.011)和-0.603(p=0.002)。

结论

IRS1 的减少与胰岛朗格汉斯区的破坏呈弱相关,表明这两个参数之间存在中间步骤。

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Indian J Clin Biochem. 2007 Sep;22(2):60-4. doi: 10.1007/BF02913315.
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The mechanisms of alloxan- and streptozotocin-induced diabetes.四氧嘧啶和链脲佐菌素诱导糖尿病的机制。
Diabetologia. 2008 Feb;51(2):216-26. doi: 10.1007/s00125-007-0886-7. Epub 2007 Dec 18.

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