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瘦素对健康大鼠和链脲佐菌素诱导的糖尿病大鼠氧化应激的影响。

Effects of leptin on oxidative stress in healthy and Streptozotocin-induced diabetic rats.

作者信息

Gülen Sebnem, Dinçer Sibel

机构信息

Department of Physiology, Faculty of Medicine, Gazi University, Ankara, Turkey.

出版信息

Mol Cell Biochem. 2007 Aug;302(1-2):59-65. doi: 10.1007/s11010-007-9426-5. Epub 2007 Feb 24.

DOI:10.1007/s11010-007-9426-5
PMID:17323002
Abstract

AIMS/HYPOTHESIS: It is generally accepted that oxidative stress is responsible for etiology and complications of diabetes. During uncontrolled Type 1 diabetes, plasma leptin levels rapidly fall. However, it is not known whether diabetes-induced hypoleptinemia has any role in oxidative stress related to uncontrolled Type I diabetes. The present study was designed to examine the effects of leptin treatment on plasma lipid peroxidation and reduced glutathion of normal and streptozotocin(STZ)-induced diabetic rats.

METHODS

Diabetes was induced by single injection of Streptozotocin (55 mg/kg bw). One week after induction of diabetes, rats began 5-day treatment protocol of leptin injections of (0.1 mg/kg bw i.p.) or same volume vehicle. At the end of the 5th day, rats were sacrificed by cardiac puncture under anesthesia and their plasma was taken for plasma leptin, malondialdehyde, and reduced glutathione measurements.

RESULTS

Plasma leptin levels decreased in STZ-induced diabetic rats while plasma glucose, TBARS, and GSH levels increased. Plasma leptin levels were not affected with leptin treatment in both diabetic and non-diabetic rats. The elevation in plasma TBARS associated with STZ diabetes decreased with leptin treatment. Leptin also increased plasma GSH levels in diabetic rats. In non-diabetic rats, treatment with leptin did not change plasma TBARS and GSH levels.

CONCLUSIONS/INTERPRETATIONS: In conclusion, leptin treatment is able to attenuate lipid peroxidation in STZ-diabetic rats, in the onset of diabetes, by increasing the GSH levels without affecting hyperglycemia and hypoleptinemia.

摘要

目的/假设:氧化应激导致糖尿病的病因和并发症,这一点已被广泛接受。在未经控制的1型糖尿病期间,血浆瘦素水平会迅速下降。然而,糖尿病诱导的低瘦素血症是否在与未经控制的1型糖尿病相关的氧化应激中起作用尚不清楚。本研究旨在检测瘦素治疗对正常大鼠和链脲佐菌素(STZ)诱导的糖尿病大鼠血浆脂质过氧化和还原型谷胱甘肽的影响。

方法

通过单次注射链脲佐菌素(55mg/kg体重)诱导糖尿病。糖尿病诱导一周后,大鼠开始为期5天的瘦素注射治疗方案(腹腔注射0.1mg/kg体重)或相同体积的赋形剂。在第5天结束时,在麻醉下通过心脏穿刺处死大鼠,并采集血浆用于检测血浆瘦素、丙二醛和还原型谷胱甘肽。

结果

STZ诱导的糖尿病大鼠血浆瘦素水平降低,而血浆葡萄糖、硫代巴比妥酸反应物(TBARS)和谷胱甘肽水平升高。瘦素治疗对糖尿病大鼠和非糖尿病大鼠的血浆瘦素水平均无影响。与STZ糖尿病相关的血浆TBARS升高在瘦素治疗后降低。瘦素还增加了糖尿病大鼠的血浆谷胱甘肽水平。在非糖尿病大鼠中,瘦素治疗未改变血浆TBARS和谷胱甘肽水平。

结论/解读:总之,在糖尿病发病初期,瘦素治疗能够通过增加谷胱甘肽水平来减轻STZ糖尿病大鼠的脂质过氧化,而不影响高血糖和低瘦素血症。

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