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[宫内生长迟缓对大鼠肝脏糖异生酶的影响]

[Effect of intrauterine growth retardation on gluconeogenic enzymes in rat liver].

作者信息

Luo Kaiju, Chen Pingyang, Xie Zongde, Li Wen, Li Suping, He Mingfeng

机构信息

Department of Neonatology, Second Xiangya Hospital, Central South University, Changsha 410011, China.

出版信息

Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2014 Apr;39(4):395-400. doi: 10.3969/j.issn.1672-7347.2014.04.013.

DOI:10.3969/j.issn.1672-7347.2014.04.013
PMID:24820282
Abstract

OBJECTIVE

To investigate the expression of gluconeogenic enzymes phosphoenolpyruvate carboxykinase (PEPCK) and G-6-Pase mRNA of hepatic tissue in rats with intrauterine growth retardation (IUGR) and to explore the molecular mechanism of insulin resistance in IUGR rats.

METHODS

Pregnant rats were randomly divided into 2 groups: a normal group and a model group. The normal group were fed with 21% protein forage and the model group with 10% low protein forage to obtain IUGR pup rats. The pup rats were introduced to the normal group and the IUGR group prospectively. At 1, 3 and 8 weeks, the body weight, blood glucose, insulin concentration and insulin resistance index of the pup rats were measured. Expression of PEPCK and G-6-Pase mRNA were detected by RT-PCR.

RESULTS

The birth weight of the IUGR group was significantly lower than that of the normal group (P<0.001). The weight of the IUGR group was still lower than that of the normal group at 1, 3 and 8 weeks. There was no significant difference in the blood glucose, insulin level and insulin resistance index between the 2 groups (P>0.05). The hepatic expression of PEPCK and G-6-Pase mRNA in the IUGR group was significantly higher than that of the normal group at 1, 3 and 8 weeks (P<0.01).

CONCLUSION

The significantly increased expression of PEPCK and G-6-Pase mRNA of hepatic tissue in IUGR rats may increase gluconeogenesis, which is probably one of the molecular mechanisms of insulin resistance and diabetes in IUGR.

摘要

目的

研究宫内生长受限(IUGR)大鼠肝组织中糖异生酶磷酸烯醇式丙酮酸羧激酶(PEPCK)和葡萄糖-6-磷酸酶(G-6-Pase)mRNA的表达,探讨IUGR大鼠胰岛素抵抗的分子机制。

方法

将孕鼠随机分为2组:正常组和模型组。正常组给予21%蛋白质饲料喂养,模型组给予10%低蛋白质饲料喂养以获得IUGR仔鼠。将仔鼠前瞻性地分为正常组和IUGR组。在1、3和8周时,测量仔鼠的体重、血糖、胰岛素浓度和胰岛素抵抗指数。通过逆转录聚合酶链反应(RT-PCR)检测PEPCK和G-6-Pase mRNA的表达。

结果

IUGR组仔鼠出生体重显著低于正常组(P<0.001)。在1、3和8周时,IUGR组仔鼠体重仍低于正常组。两组血糖、胰岛素水平和胰岛素抵抗指数差异无统计学意义(P>0.05)。在1、3和8周时,IUGR组肝组织中PEPCK和G-6-Pase mRNA的表达显著高于正常组(P<0.01)。

结论

IUGR大鼠肝组织中PEPCK和G-6-Pase mRNA表达显著增加可能增强糖异生作用,这可能是IUGR大鼠胰岛素抵抗和糖尿病的分子机制之一。

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