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

doi:10.3969/j.issn.1674-5817.2015.03.001

Abstract

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

CLC Number:

Q95-33

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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