Objective：This study compared the expression spectrum of long noncoding RNA（lncRNA） and messenger RNA（mRNA）in pancreatic tissue between intrauterine growth retardation（IUGR）and normal neonatal mice，and then explored the potential mechanism of islet developmental disorders in IUGR mice and development of diabetes later in their adulthood. Methods：IUGR and normal neonatal mice models were established，whole transcriptome sequencing in pancreas of two groups were performed，and then gene ontology（GO）and Kyoto Encyclopedia of gene and genomes（KEEG）enrichment analysis were conducted. To further analyse the whole transcriptome sequencing information，we selected several lncRNAs with high differential expression for validation，which were also reported to be involved in islet development. Results：Total 294 lncRNAs were differentially expressed between IUGR and normal neonatal mice，among which 83 were up-regulated and 211 were down-regulated. There were 2 000 differentially expressed mRNAs，of which 1 711 were up-regulated and 289 were down-regulated. The GO analysis of lncRNA target genes and differential mRNAs showed：biological pathways（BP）are concentrated in cellular processes，biological regulation and metabolic processes；cell components（CC）are concentrated in cell and organ processes；molecular function（MF）mainly focuses on integration，catalytic activity，transportation activity，etc. KEEG enrichment analysis highlights the involvement of PI3K-Akt pathway，MAPK pathway and Foxo pathway. Through verified experiments，the selected lncRNA Snhg12 and Rian showed significant differences between IUGR mice and normal mice，which is consistent with the sequencing results，and the expression were regulated by glucose concentration. Conclusion：This study analyzed and partially verified the lncRNA and mRNA differentially expressed in IUGR，which is helpful to explore the potential mechanism of islet developmental disorders and later adult diabetes in mice born with IUGR，especially the role of lncRNAs.