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Journal of Biomedicine and Biotechnology
Volume 2005 (2005), Issue 2, Pages 104-112
Research article

Data-Mining Analysis Suggests an Epigenetic Pathogenesis for Type 2 Diabetes

1Advanced Center for Genome Technology, Department of Botany and Microbiology, The University of Oklahoma, 101 David L Boren Blvd, Rm 2025, Norman, OK 73019, USA
2The McDermott Center for Human Growth and Development, The University of Texas Southwestern Medical Center, 6000 Harry Hines Blvd, Dallas, TX 75390-8591, USA
3Departments of Biochemistry and Internal Medicine and Center for Biomedical Inventions, The University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390, USA

Received 28 April 2004; Revised 3 August 2004; Accepted 9 August 2004

Copyright © 2005 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The etiological origin of type 2 diabetes mellitus (T2DM) has long been controversial. The body of literature related to T2DM is vast and varied in focus, making a broad epidemiological perspective difficult, if not impossible. A data-mining approach was used to analyze all electronically available scientific literature, over 12 million Medline records, for “objects” such as genes, diseases, phenotypes, and chemical compounds linked to other objects within the T2DM literature but were not themselves within the T2DM literature. The goal of this analysis was to conduct a comprehensive survey to identify novel factors implicated in the pathology of T2DM by statistically evaluating mutually shared associations. Surprisingly, epigenetic factors were among the highest statistical scores in this analysis, strongly implicating epigenetic changes within the body as causal factors in the pathogenesis of T2DM. Further analysis implicates adipocytes as the potential tissue of origin, and cytokines or cytokine-like genes as the dysregulated factor(s) responsible for the T2DM phenotype. The analysis provides a wealth of literature supporting this hypothesis, which—if true—represents an important paradigm shift for researchers studying the pathogenesis of T2DM.