PMID- 35241929
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220502
IS  - 1178-7074 (Print)
IS  - 1178-7074 (Electronic)
IS  - 1178-7074 (Linking)
VI  - 15
DP  - 2022
TI  - Downregulation of ALDH6A1 is a New Marker of Muscle Insulin Resistance in Type 2 
      Diabetes Mellitus.
PG  - 2137-2147
LID - 10.2147/IJGM.S343727 [doi]
AB  - PURPOSE: Skeletal muscle insulin resistance (IR) is an important etiology of type 
      2 diabetes mellitus (T2DM); however, its molecular mechanism is yet to be fully 
      defined. This study attempted to identify the gene expression patterns and 
      molecular disorders in T2DM patients' skeletal muscle samples. METHODS: First, 
      the difference in genetic expression among GSE25462 data was analyzed. Next, PPI 
      network analysis of differential genes was carried out, after which the 
      maladjustment module was identified. Then, an enrichment analysis and gene set 
      enrichment analysis (GSEA) were carried out. Finally, the transcription factors 
      that regulate the modular genes by raid were predicted. RESULTS: Most 
      differentially expressed genes were found to be able to form an interaction 
      network and cluster into 9 modules. These modular genes were shown to possess a 
      significant correlation with immune inflammation and metabolic response. 
      Importantly, the top 15 genes of area under receiver operating characteristic 
      curve (AUC) were identified, and the expression of 10 genes by GSE12643, GSE18732 
      and GSE29221 was confirmed. The expression and AUC value of ALDH6A1 were then 
      verified according to three sets of data, where ALDH6A1 was found to be 
      negatively correlated with follicular helper T cells. However, among the 
      predicted transcription regulators, HDAC was shown to have a better regulatory 
      effect. CONCLUSION: The findings highlight that the dysregulation of ALDH6A1 
      expression in IR of T2DM may serve as a potential therapeutic target. ALDH6A1 is 
      involved in the immune inflammation and metabolic pathways.
CI  - (c) 2022 Liu et al.
FAU - Liu, Song
AU  - Liu S
AD  - Endocrinology Department, Traditional Chinese Medicine Academy of Heilongjiang, 
      Harbin, Heilongjiang Province, People's Republic of China.
FAU - Cai, Xiaojun
AU  - Cai X
AD  - Endocrinology Department, Traditional Chinese Medicine Academy of Heilongjiang, 
      Harbin, Heilongjiang Province, People's Republic of China.
FAU - Wang, Tao
AU  - Wang T
AD  - Endocrinology Department, Traditional Chinese Medicine Academy of Heilongjiang, 
      Harbin, Heilongjiang Province, People's Republic of China.
FAU - Xu, Jiwen
AU  - Xu J
AD  - Anatomy, Histology and Embryology Teaching and Research Section, School of Basic 
      Medicine, Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang 
      Province, People's Republic of China.
FAU - Cheng, Weilun
AU  - Cheng W
AD  - Department of General Surgery, The First Affiliated Hospital of Harbin Medical 
      University, Harbin, Heilongjiang Province, People's Republic of China.
FAU - Wang, Xuling
AU  - Wang X
AD  - Endocrinology Department, Traditional Chinese Medicine Academy of Heilongjiang, 
      Harbin, Heilongjiang Province, People's Republic of China.
FAU - Wei, Gangjie
AU  - Wei G
AD  - Medical Department, Traditional Chinese Medicine Academy of Heilongjiang, Harbin, 
      Heilongjiang Province, People's Republic of China.
FAU - Yan, Shuang
AU  - Yan S
AD  - Department of Endocrinology and Metabolism, The Fourth Affiliated Hospital of 
      Harbin Medical University, Harbin, Heilongjiang Province, People's Republic of 
      China.
LA  - eng
PT  - Journal Article
DEP - 20220225
PL  - New Zealand
TA  - Int J Gen Med
JT  - International journal of general medicine
JID - 101515487
PMC - PMC8887615
OTO - NOTNLM
OT  - ALDH6A1
OT  - HDAC
OT  - immune inflammatory response
OT  - metabolic pathway
OT  - type 2 diabetes mellitus
COIS- The authors declare that there are no conflicts of interest among the authors 
      regarding the publication of this paper.
EDAT- 2022/03/05 06:00
MHDA- 2022/03/05 06:01
PMCR- 2022/02/25
CRDT- 2022/03/04 05:39
PHST- 2021/10/27 00:00 [received]
PHST- 2022/01/21 00:00 [accepted]
PHST- 2022/03/04 05:39 [entrez]
PHST- 2022/03/05 06:00 [pubmed]
PHST- 2022/03/05 06:01 [medline]
PHST- 2022/02/25 00:00 [pmc-release]
AID - 343727 [pii]
AID - 10.2147/IJGM.S343727 [doi]
PST - epublish
SO  - Int J Gen Med. 2022 Feb 25;15:2137-2147. doi: 10.2147/IJGM.S343727. eCollection 
      2022.