Targets and Candidate Agents for Type 2 Diabetes Treatment with Computational Bioinformatics Approach

Journal of Diabetes Research. 2014;2014 DOI 10.1155/2014/763936

 

Journal Homepage

Journal Title: Journal of Diabetes Research

ISSN: 2314-6745 (Print); 2314-6753 (Online)

Publisher: Hindawi Limited

LCC Subject Category: Medicine: Internal medicine: Specialties of internal medicine: Diseases of the endocrine glands. Clinical endocrinology

Country of publisher: United Kingdom

Language of fulltext: English

Full-text formats available: PDF, HTML, ePUB, XML

 

AUTHORS


Qiong Wang (Department of Endocrinology, Henan Provincial People’s Hospital, No. 7 Weiwu Road, Zhengzhou 450003, China)

Zhigang Zhao (Department of Endocrinology, Henan Provincial People’s Hospital, No. 7 Weiwu Road, Zhengzhou 450003, China)

Jing Shang (Department of Endocrinology, Henan Provincial People’s Hospital, No. 7 Weiwu Road, Zhengzhou 450003, China)

Wei Xia (Department of Endocrinology, Henan Provincial People’s Hospital, No. 7 Weiwu Road, Zhengzhou 450003, China)

EDITORIAL INFORMATION

Blind peer review

Editorial Board

Instructions for authors

Time From Submission to Publication: 14 weeks

 

Abstract | Full Text

We sought to explore the molecular mechanism of type 2 diabetes (T2D) and identify potential drug targets and candidate agents for T2D treatment. The differentially expressed genes (DEGs) were assessed between human pancreatic islets with T2D and normal islets. The dysfunctional pathways, the potential transcription factor, and microRNA targets were analyzed by bioinformatics methods. Moreover, a group of bioactive small molecules were identified based on the connectivity map database. The pathways of Eicosanoid Synthesis, TGF-beta signaling pathway, Prostaglandin Synthesis and Regulation, and Integrated Pancreatic Cancer Pathway were found to be significantly dysregulated in the progression of T2D. The genes of ZADH2 (zinc binding alcohol dehydrogenase domain containing 2), BTBD3 (BTB (POZ) domain containing 3), Cul3-based ligases,  LTBP1 (latent-transforming growth factor beta binding protein 1), PDGFRA (alpha-type platelet-derived growth factor receptor), and FST (follistatin) were determined to be significant nodes regulated by potential transcription factors and microRNAs. Besides, two small molecules (sanguinarine and DL-thiorphan) were identified to be capable of reverse T2D. In the present study, a systematic understanding for the mechanism underlying T2D development was provided with biological informatics methods. The significant nodes and bioactive small molecules may be drug targets and candidate agents for T2D treatment.