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首页> 外文期刊>Cell biology international. >Changes in liver gangliosides in streptozotocin-induced diabetic rats.
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Changes in liver gangliosides in streptozotocin-induced diabetic rats.

机译：链脲佐菌素诱导的糖尿病大鼠肝脏神经节苷脂的变化。

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摘要

Diabetes mellitus is associated with various structural and functional liver abnormalities that affect the glycogen and lipid metabolisms. The effects of streptozotocin-induced diabetes and of insulin supplementation to Sprague-Dawley diabetic rats on ganglioside patterns in liver were determined. Diabetic livers showed a tendency to hepatomegaly 3 weeks after STZ-induction of diabetes. The concentration of total gangliosides in diabetic and non-diabetic livers was similar, but the concentration of total gangliosides in the liver of insulin-stabilized rats was slightly increased. Bidimensional TLC chromatographic analysis of gangliosides isolated from normal diabetic and insulin-stabilized diabetic livers showed quantitative and qualitative changes. In comparison with normal controls, the densitometric analyses of diabetic liver ganglioside patterns had increased amounts of GM3, GM1, GD1b, and GT1b gangliosides, while GM2 could not be detected. The hepatic ganglioside pattern of insulin-stabilized diabetic rats was partially restored, resembling the profile of normal rats. The activity of GalNAcT, GalT-2 and SialT-4 transferases was measured in liver microsomal fractions of the different groups of animals. Diabetic rats showed an increased activity of GalNAcT and a decrease in the activity of GalT-2 and SialT-4 compared with the controls. The enzymatic activities found in insulin-treated rats showed a tendency to return to the values observed in normal control animals. The results evidenced that streptozotocin-induced diabetes affects the liver ganglioside pattern and the ganglioside synthesis enzyme activity. The alterations found in ganglioside metabolism could represent one of the earliest changes associated with the diabetic pathology. Copyright 2000 Academic Press.
机译：糖尿病与影响糖原和脂质代谢的各种肝脏结构和功能异常有关。确定了链脲佐菌素诱导的糖尿病和对Sprague-Dawley糖尿病大鼠补充胰岛素对肝脏神经节苷脂模式的影响。在STZ诱导糖尿病后3周，糖尿病肝脏表现出肝肿大的趋势。糖尿病和非糖尿病肝脏中总神经节苷脂的浓度相似，但胰岛素稳定大鼠肝脏中总神经节苷脂的浓度略有增加。从正常糖尿病和胰岛素稳定的糖尿病肝脏中分离出的神经节苷脂的二维TLC色谱分析显示出定量和定性的变化。与正常对照相比，糖尿病肝神经节苷脂模式的光密度分析增加了GM3，GM1，GD1b和GT1b神经节苷脂的量，而无法检测到GM2。胰岛素稳定的糖尿病大鼠的肝神经节苷脂模式被部分恢复，类似于正常大鼠的轮廓。在不同组动物的肝微粒体级分中测量了GalNAcT，GalT-2和SialT-4转移酶的活性。与对照组相比，糖尿病大鼠显示出GalNAcT活性增加，而GalT-2和SialT-4活性降低。在用胰岛素治疗的大鼠中发现的酶活性显示出恢复到正常对照动物中观察到的值的趋势。结果证明，链脲佐菌素诱发的糖尿病会影响肝脏神经节苷脂模式和神经节苷脂合成酶活性。神经节苷脂代谢中发现的改变可能是与糖尿病病理相关的最早改变之一。版权所有2000学术出版社。

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