PMID- 27906902
OWN - NLM
STAT- MEDLINE
DCOM- 20170329
LR  - 20190606
IS  - 1643-3750 (Electronic)
IS  - 1234-1010 (Print)
IS  - 1234-1010 (Linking)
VI  - 22
DP  - 2016 Dec 1
TI  - Comparison of Transcriptome Between Type 2 Diabetes Mellitus and Impaired Fasting 
      Glucose.
PG  - 4699-4706
AB  - BACKGROUND The aim of this study was to compare the transcriptome between 
      impaired fasting glucose (IFG) and type 2 diabetes mellitus (T2DM), and further 
      research their molecular mechanisms. MATERIAL AND METHODS The original microarray 
      GSE21321, including miRNA and mRNA expression profiles, was downloaded from the 
      GEO database. Data preprocessing was processed by limma package, and 
      differentially expressed genes (DGs) and miRNA (DMs) were screened. Then, the 
      regulatory relationships among miRNA, TF, and genes were screened and the 
      regulatory network was constructed. Finally, DAVID was used for KEGG enrichment 
      analysis. RESULTS There were 11 upregulated IFG-related DMs and five upregulated 
      T2DM-related DMs. Three of the DMs overlapped. In addition, there were eight 
      downregulated IFG-related DMs and two downregulated T2DM-related DMs. Only one 
      downregulated DM overlapped. Similarly, there were 264 upregulated IFG-related 
      DGs and 331 upregulated T2DM-related DGs; and 196 overlapping genes were 
      obtained. In addition, there were 400 downregulated IFG-related DMs and 568 
      downregulated T2DM-related DMs. A total of 326 downregulated DMs were overlapped. 
      The overlapped DGs were enriched in various pathways, including hematopoietic 
      cell lineage, Fc gamma R-mediated phagocytosis, and MAPK signaling pathway. TAF1 
      (upregulated gene) and MAFK (downregulated gene) were hub nodes both in IFG- and 
      T2DM-related miRNA-TF-gene regulatory network. In addition, miRNAs, including 
      hsa-miR-29a, hsa-miR-192, and hsa-miR-144, were upregulated hub nodes in the two 
      regulatory networks. CONCLUSIONS Genes including TAF1 and MAFK, and miRNAs 
      including hsa-miR-29a, hsa-miR-192, and hsa-miR-144 might be potential target 
      genes and important miRNAs for IFG and T2DM.
FAU - Cui, Ying
AU  - Cui Y
AD  - Department of Endocrinology, Jinan Central Hospital Affiliated to Shandong 
      University, Jinan, Shandong, China (mainland)
FAU - Chen, Wen
AU  - Chen W
AD  - Department of Neurology, Jinan Central Hospital Affiliated to Shandong 
      University, Jinan, Shandong, China (mainland)
FAU - Chi, Jinfeng
AU  - Chi J
AD  - Department of Endocrinology, Jinan Central Hospital Affiliated to Shandong 
      University, Jinan, Shandong, China (mainland)
FAU - Wang, Lei
AU  - Wang L
AD  - Department of Cardiology, Jinan Central Hospital Affiliated to Shandong 
      University, Jinan, Shandong, China (mainland)
LA  - eng
PT  - Comparative Study
PT  - Journal Article
DEP - 20161201
PL  - United States
TA  - Med Sci Monit
JT  - Medical science monitor : international medical journal of experimental and 
      clinical research
JID - 9609063
RN  - 0 (Blood Glucose)
RN  - 0 (MAFK protein, human)
RN  - 0 (MafK Transcription Factor)
RN  - 0 (MicroRNAs)
RN  - 0 (TATA-Binding Protein Associated Factors)
RN  - 0 (Transcription Factor TFIID)
RN  - EC 2.3.1.48 (Histone Acetyltransferases)
RN  - EC 2.7.11.1 (TATA-binding protein associated factor 250 kDa)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Blood Glucose/metabolism
MH  - Case-Control Studies
MH  - Diabetes Mellitus, Type 2/blood/*genetics/metabolism
MH  - Fasting/metabolism/*physiology
MH  - Gene Expression Profiling/*methods
MH  - Gene Expression Regulation
MH  - Glucose/metabolism
MH  - Histone Acetyltransferases/genetics/metabolism
MH  - Humans
MH  - MAP Kinase Signaling System
MH  - MafK Transcription Factor/genetics/metabolism
MH  - Male
MH  - MicroRNAs/biosynthesis/*genetics
MH  - Middle Aged
MH  - TATA-Binding Protein Associated Factors/genetics/metabolism
MH  - Transcription Factor TFIID/genetics/metabolism
MH  - Transcriptome
PMC - PMC5147684
COIS- Conflict of interests All authors declare that they have no conflict of interests 
      to state.
EDAT- 2016/12/03 06:00
MHDA- 2017/03/31 06:00
PMCR- 2016/12/01
CRDT- 2016/12/02 06:00
PHST- 2016/12/02 06:00 [entrez]
PHST- 2016/12/03 06:00 [pubmed]
PHST- 2017/03/31 06:00 [medline]
PHST- 2016/12/01 00:00 [pmc-release]
AID - 896772 [pii]
AID - 10.12659/msm.896772 [doi]
PST - epublish
SO  - Med Sci Monit. 2016 Dec 1;22:4699-4706. doi: 10.12659/msm.896772.