PMID- 37534872
OWN - NLM
STAT- MEDLINE
DCOM- 20231216
LR  - 20231216
IS  - 2724-6116 (Electronic)
IS  - 2724-6116 (Linking)
VI  - 48
IP  - 4
DP  - 2023 Dec
TI  - Exploration of the molecular mechanism of insulin resistance in adipose tissue of 
      patients with type 2 diabetes mellitus through a bioinformatic analysis.
PG  - 440-446
LID - 10.23736/S2724-6507.22.03771-X [doi]
AB  - BACKGROUND: We aimed to determine the cis-expression Quantitative Trait Loci 
      (cis-eQTL) and trans-eQTL of differentially expressed genes (DEGs) in insulin 
      resistance (IR) related pathways. METHODS: The expression profile data for 
      insulin sensitivity (IS) and IR in the adipose tissue of patients with type 2 
      diabetes mellitus (T2DM) were acquired from the Gene Expression Omnibus 
      databases. Then, the Gene set enrichment analysis (GSEA) and Gene set variation 
      analysis (GSVA) methods were performed to identify the significant enrichment of 
      potential Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways between IS and 
      IR groups, and the Wilcoxon rank sum test was carried out to identify the DEGs 
      related to KEGG pathways. Finally, the cis-eQTLs and trans-eQTLs that can affect 
      the expression of DEGs were screened from the eQTLGen database. RESULTS: The GSEA 
      and GSVA analysis indicated that the mTOR signaling pathway, insulin signaling 
      pathway and T2DM had a strong correlation with the pathological process of T2DM. 
      Furthermore, six genes (ACACA, GYS2, PCK1, PRKAR1A, SLC2A4, and VEGFA) were found 
      to be significantly differentially expressed in IR-related pathways. Finally, we 
      have identified a total of 1073 cis-eQTLs and 24 trans-eQTLs. CONCLUSIONS: We 
      screened out six genes that were significantly differentially expressed in 
      IR-related pathways, including ACACA, GYS2, PCK1, PRKAR1A, SLC2A4, and VEGFA. 
      Moreover, we discovered that these six genes were affected by 1073 cis-eQTLs and 
      24 trans-eQTLs.
FAU - Wang, Yujing
AU  - Wang Y
AD  - Department of Endocrinology, The Fourth Affiliated Hospital of Harbin Medical 
      University, Harbin, China.
FAU - Zhou, Weiyu
AU  - Zhou W
AD  - Department of Endocrinology, The Fourth Affiliated Hospital of Harbin Medical 
      University, Harbin, China.
FAU - Liu, Dana
AU  - Liu D
AD  - Department of Endocrinology, The First Hospital, Harbin, China.
FAU - Zhang, Zhiying
AU  - Zhang Z
AD  - Department of Endocrinology, The Fourth Affiliated Hospital of Harbin Medical 
      University, Harbin, China.
FAU - Xu, Yuanxin
AU  - Xu Y
AD  - Department of Endocrinology, The Fourth Affiliated Hospital of Harbin Medical 
      University, Harbin, China.
FAU - Wan, Xiaojing
AU  - Wan X
AD  - Department of Endocrinology, The Fourth Affiliated Hospital of Harbin Medical 
      University, Harbin, China.
FAU - Yu, Haiqiao
AU  - Yu H
AD  - Department of Endocrinology, The Fourth Affiliated Hospital of Harbin Medical 
      University, Harbin, China.
FAU - Yan, Shuang
AU  - Yan S
AD  - Department of Endocrinology, The Fourth Affiliated Hospital of Harbin Medical 
      University, Harbin, China - qingmei0742_1@163.com.
LA  - eng
PT  - Journal Article
DEP - 20230803
PL  - Italy
TA  - Minerva Endocrinol (Torino)
JT  - Minerva endocrinology
JID - 101777342
SB  - IM
MH  - Humans
MH  - *Insulin Resistance/genetics
MH  - *Diabetes Mellitus, Type 2/genetics
MH  - Computational Biology/methods
MH  - Adipose Tissue/metabolism
MH  - Quantitative Trait Loci/genetics
EDAT- 2023/08/03 13:09
MHDA- 2023/12/17 09:46
CRDT- 2023/08/03 08:46
PHST- 2023/12/17 09:46 [medline]
PHST- 2023/08/03 13:09 [pubmed]
PHST- 2023/08/03 08:46 [entrez]
AID - S2724-6507.22.03771-X [pii]
AID - 10.23736/S2724-6507.22.03771-X [doi]
PST - ppublish
SO  - Minerva Endocrinol (Torino). 2023 Dec;48(4):440-446. doi: 
      10.23736/S2724-6507.22.03771-X. Epub 2023 Aug 3.