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从链脲佐菌素诱导的糖尿病大鼠分离出的II型肺细胞中磷脂生物合成的改变。

Altered phospholipid biosynthesis in type II pneumocytes isolated from streptozotocin-diabetic rats.

作者信息

Uhal B D, Longmore W J

出版信息

Biochim Biophys Acta. 1986 Sep 12;878(2):266-72. doi: 10.1016/0005-2760(86)90155-4.

DOI:10.1016/0005-2760(86)90155-4
PMID:3530333
Abstract

To determine whether type II pneumocytes isolated from diabetic animals could serve as a useful model for the study of surfactant phospholipid biosynthesis and its regulation, type II pneumocytes were isolated from adult streptozotocin-diabetic rats and placed in short-term primary culture. On a DNA basis, total cellular disaturated phosphatidylcholine (disaturated PC) and phosphatidylglycerol (PG) were decreased 36 and 66%, respectively, in type II cells from diabetic animals. 7 days of insulin treatment of diabetic rats returned the cellular disaturated PC and PG content to control values and increased the total cellular phosphatidylethanolamine (PE) content by 51%. The rates of glucose and acetate incorporation into disaturated PC per unit DNA were reduced 32 and 38%, respectively, in cells isolated from diabetic rats, while glycerol incorporation was increased by 143%. Insulin treatment of diabetic rats returned the glucose and glycerol incorporation rates to control values and increased acetate incorporation into disaturated PC by 66%. These data suggest that the biosynthesis of surfactant is altered by both diabetes mellitus and in vivo insulin treatment.

摘要

为了确定从糖尿病动物分离出的II型肺细胞是否可作为研究表面活性物质磷脂生物合成及其调节的有用模型,从成年链脲佐菌素诱导的糖尿病大鼠中分离出II型肺细胞,并进行短期原代培养。以DNA为基础,糖尿病动物的II型细胞中,总细胞双饱和磷脂酰胆碱(双饱和PC)和磷脂酰甘油(PG)分别减少了36%和66%。对糖尿病大鼠进行7天的胰岛素治疗后,细胞双饱和PC和PG含量恢复到对照值,并且总细胞磷脂酰乙醇胺(PE)含量增加了51%。从糖尿病大鼠分离出的细胞中,每单位DNA的葡萄糖和乙酸盐掺入双饱和PC的速率分别降低了32%和38%,而甘油掺入增加了143%。对糖尿病大鼠进行胰岛素治疗后,葡萄糖和甘油掺入速率恢复到对照值,并且乙酸盐掺入双饱和PC增加了66%。这些数据表明,糖尿病和体内胰岛素治疗均会改变表面活性物质的生物合成。

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Altered phospholipid biosynthesis in type II pneumocytes isolated from streptozotocin-diabetic rats.从链脲佐菌素诱导的糖尿病大鼠分离出的II型肺细胞中磷脂生物合成的改变。
Biochim Biophys Acta. 1986 Sep 12;878(2):266-72. doi: 10.1016/0005-2760(86)90155-4.
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