肥胖相关糖尿病内脏脂肪组织关键通路的基因组分析和鉴定

Yue Shi, Wentao Han, Huagen Wei, Siwei Zhou, Weizheng Kong, Li-ping Shi, Huiqun Wu
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引用次数: 0

摘要

肥胖会增加患糖尿病的风险;然而,并不是每个肥胖的人都会患上糖尿病。本研究从基因表达综合数据库(Gene Expression Omnibus database, GEO)下载数据集GSE54350,包括肥胖糖尿病和非糖尿病样本作为对照。使用GEO2R插件选择肥胖糖尿病和非糖尿病样本之间的差异表达基因(DEGs)。基因本体(GO)富集和蛋白-蛋白相互作用(PPI)分析使用metscape。结果显示,共有1073个基因,其中上调基因496个,下调基因577个。这些deg在止血、细胞器组装调节、凋亡信号传导、髓系白细胞活化、细胞凋亡等生物学途径中富集。我们发现Caspase 3 (CASP3)和组织金属蛋白酶3抑制剂(TIMP3)可能是肥胖相关性糖尿病的标记基因和潜在的治疗靶点,值得进一步研究验证。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Genome analysis and identification of key pathway in visceral adipose tissue from obesity-related diabetes
Obesity increases the risk of diabetes; however, not everyone who is obese develops diabetes. In this study, the dataset GSE54350 was downloaded from the Gene Expression Omnibus database (GEO), including obese diabetic and non-diabetic samples as control. Differentially expressed genes (DEGs) between obese diabetic and non-diabetic samples were selected using GEO2R plugin. Gene ontology (GO) enrichment and protein-protein interaction (PPI) analysis of these DEGs were performed using Metascape. The results showed 1073 DEGs, including 496 up-regulated genes and 577 down-regulated genes. These DEGs were enriched in biological pathways involved in hemostasis, regulation of organelle assembly, apoptotic signaling, myeloid leukocyte activation, apoptosis, etc. We revealed that Caspase 3 (CASP3) and tissue inhibitor of metalloproteinase 3 (TIMP3) might serve as marker genes and potential therapeutic targets for obesity-related diabetes, which deserves further investigations for validation.
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