PMID- 31524257 OWN - NLM STAT- MEDLINE DCOM- 20200204 LR - 20200225 IS - 1791-3004 (Electronic) IS - 1791-2997 (Print) IS - 1791-2997 (Linking) VI - 20 IP - 3 DP - 2019 Sep TI - Identification of core genes and pathways in type 2 diabetes mellitus by bioinformatics analysis. PG - 2597-2608 LID - 10.3892/mmr.2019.10522 [doi] AB - Type 2 diabetes mellitus (T2DM) is a metabolic disorder. Numerous proteins have been identified that are associated with the occurrence and development of T2DM. This study aimed to identify potential core genes and pathways involved in T2DM, through exhaustive bioinformatic analyses using GSE20966 microarray profiles of pancreatic beta‑cells obtained from healthy controls and patients with T2DM. The original microarray data were downloaded from the Gene Expression Omnibus database. Data were processed by the limma package in R software and the differentially expressed genes (DEGs) were identified. Gene Ontology functional analysis and Kyoto Encyclopedia of Genes and Genomes pathway analysis were carried out to identify potential biological functions and pathways of the DEGs. Key transcription factors were identified using the WEB‑based GEne SeT AnaLysis Toolkit (WebGestalt) and Enrichr. The Search Tool for the Retrieval of Interacting Genes (STRING) database was used to establish a protein‑protein interaction (PPI) network for the DEGs. In total, 329 DEGs were involved in T2DM, with 208 upregulated genes enriched in pancreatic secretion and the complement and coagulation cascades, and 121 downregulated genes enriched in insulin secretion, carbohydrate digestion and absorption, and the Toll‑like receptor pathway. Furthermore, hepatocyte nuclear factor 1‑alpha (HNF1A), signal transducer and activator of transcription 3 (STAT3) and glucocorticoid receptor (GR) were key transcription factors in T2DM. Twenty important nodes were detected in the PPI network. Finally, two core genes, serpin family G member 1 (SERPING1) and alanyl aminopeptidase, membrane (ANPEP), were shown to be associated with the development of T2DM. On the whole, the findings of this study enhance our understanding of the potential molecular mechanisms of T2DM and provide potential targets for further research. FAU - Ding, Linchao AU - Ding L AD - Department of Scientific Research, Jinhua Hospital, Zhejiang University School of Medicine, Jinhua, Zhejiang 321000, P.R. China. FAU - Fan, Lei AU - Fan L AD - Department of Pharmacy, Jinhua Hospital, Zhejiang University School of Medicine, Jinhua, Zhejiang 321000, P.R. China. FAU - Xu, Xiaodong AU - Xu X AD - Department of Endocrinology, Jinhua Hospital, Zhejiang University School of Medicine, Jinhua, Zhejiang 321000, P.R. China. FAU - Fu, Jianfei AU - Fu J AD - Department of Scientific Research, Jinhua Hospital, Zhejiang University School of Medicine, Jinhua, Zhejiang 321000, P.R. China. FAU - Xue, Yadong AU - Xue Y AD - Department of Scientific Research, Jinhua Hospital, Zhejiang University School of Medicine, Jinhua, Zhejiang 321000, P.R. China. LA - eng PT - Journal Article DEP - 20190724 PL - Greece TA - Mol Med Rep JT - Molecular medicine reports JID - 101475259 RN - 0 (Biomarkers) SB - IM MH - Animals MH - Biomarkers MH - Cell Line MH - *Computational Biology/methods MH - Databases, Genetic MH - Diabetes Mellitus, Type 2/*genetics/*metabolism MH - Disease Susceptibility MH - *Gene Expression Regulation MH - Gene Ontology MH - Gene Regulatory Networks MH - Humans MH - Mice MH - *Signal Transduction PMC - PMC6691242 EDAT- 2019/09/17 06:00 MHDA- 2020/02/06 06:00 PMCR- 2019/07/24 CRDT- 2019/09/17 06:00 PHST- 2019/01/10 00:00 [received] PHST- 2019/05/07 00:00 [accepted] PHST- 2019/09/17 06:00 [pubmed] PHST- 2020/02/06 06:00 [medline] PHST- 2019/09/17 06:00 [entrez] PHST- 2019/07/24 00:00 [pmc-release] AID - mmr-20-03-2597 [pii] AID - 10.3892/mmr.2019.10522 [doi] PST - ppublish SO - Mol Med Rep. 2019 Sep;20(3):2597-2608. doi: 10.3892/mmr.2019.10522. Epub 2019 Jul 24.