Hnrnpu+/-小鼠表现出发育迟缓、活动水平下降和糖代谢异常

doi:10.3969/j.issn.1674-5817.2015.03.001

实验动物与比较医学 ›› 2015, Vol. 35 ›› Issue (3): 175-181.DOI: 10.3969/j.issn.1674-5817.2015.03.001

所属专题：实验动物资源开发与利用

• 论著 • 下一篇

Hnrnpu^+/-小鼠表现出发育迟缓、活动水平下降和糖代谢异常

孙敏^1,2, 沙海波², 屠鑫², 邹耩欢², 赖贝贝², 高翔^1,2, 齐心²

1.上海交通大学医学院医学遗传学教研室, 上海200025;
2.南京大学模式动物研究所教育部重点实验室, 南京210061

收稿日期:2014-09-26 出版日期:2015-06-25 发布日期:2015-06-25
作者简介:孙敏(1989-), 女, 硕士, 研究方向: 实验动物遗传学, E-mail: sunmin@nicemice.cn
基金资助:
国家重点基础研究发展计划(973计划)(2011CB944104)和国家科技支撑计划(2011BAI15B02; 2012BAI39B01)

hnRNP U Haploinsufficiency Leads to Growth Retardation, Decreased Activities and Abnormal Glucose Metabolism in Mice

SUN Min^1,2, SHA Hai-bo², TU Xin², ZOU Jiang-huan², LAI Bei-bei², GAO Xiang^1,2, QI Xin²

1. Department of Medical Genetics Shanghai Jiao Tong University School of Medicine, Shanghai, 200025. China;
2. MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing University, Nanjing 210061, China

Received:2014-09-26 Online:2015-06-25 Published:2015-06-25

摘要/Abstract

摘要： 目的建立核异质核糖核蛋白U(hnRNP U)基因全身性敲除小鼠模型,研究该基因在小鼠体内的功能。方法通过同源重组的方法建立hnRNP U全身性敲除的小鼠模型。观察统计小鼠的出生以及生长情况,检查其组织器官发育,通过代谢笼检测其代谢水平,并用糖耐量试验检测其糖代谢变化。结果 hnRNP U全身性敲除纯合子小鼠(Hnrnpu^-/-)死于胚胎期7.5 d前,而其杂合子小鼠也有部分在胚胎期死亡,出生的杂合子小鼠表现为生长发育迟缓、部分组织的重量减轻、骨密度降低以及肌肉含量减少。进一步实验表明,Hnrnpu^+/-小鼠夜间进食量、活动水平和产热量等降低,糖代谢能力下降。结论通过同源重组方法成功建立hnRNP U全身性敲除小鼠模型,并在整体水平证实了该基因在小鼠发育和代谢稳态调节中起重要作用。

关键词: 核异质核糖核蛋白U(hnRNP U), 基因敲除, 发育迟缓, 代谢异常, 糖代谢

Abstract: Objective To establish a heterogeneous nuclear ribonucleoprotein U (HnRNP U) knockout mouse model and study the roles of hnRNP U in vivo. Methods The Hnrnpu conventional knockout mouse model was established by homologous recombination. The roles of hnRNP U in vivo were studied by growth analyses, body and tissues weighting, metabolic analyses and glucose tolerance tests. Results The Hnrnpu^-/- mice are embryonic leathal before embryonic day 7.5. The Hnrnpu^+/- mice were partially died at embryonic stage and the viable individuals showed growth retardation with decreased tissues weight, bone mineral density and lean mass compared with wild-type littermates. In addition, hnRNP U haploinsufficiency leads to decreased activity and food intake at night and impaired glucose homeostasis. Conclusion Hnrnpu knockout mouse model was successfully established and hnRNP U played a great role in a diverse group of cellular processes, including the normal growth of somatic tissues, metabolic activities and glucose metabolism.

Key words: Heterogeneous nuclear ribonucleoprotein U (hnRNP U), Knockout, Growth retardation, Metabolic disorder, Glucose metabolism

中图分类号:

Q95-33

孙敏, 沙海波, 屠鑫, 邹耩欢, 赖贝贝, 高翔, 齐心. Hnrnpu^+/-小鼠表现出发育迟缓、活动水平下降和糖代谢异常[J]. 实验动物与比较医学, 2015, 35(3): 175-181.

SUN Min, SHA Hai-bo, TU Xin, ZOU Jiang-huan, LAI Bei-bei, GAO Xiang, QI Xin. hnRNP U Haploinsufficiency Leads to Growth Retardation, Decreased Activities and Abnormal Glucose Metabolism in Mice[J]. Laboratory Animal and Comparative Medicine, 2015, 35(3): 175-181.

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Hnrnpu^+/-小鼠表现出发育迟缓、活动水平下降和糖代谢异常

hnRNP U Haploinsufficiency Leads to Growth Retardation, Decreased Activities and Abnormal Glucose Metabolism in Mice

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