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Minireview: The Wnt Signaling Pathway Effector TCF7L2 and Type 2 Diabetes Mellitus

Departments of Medicine, Physiology, and Laboratory Medicine and Pathobiology, University of Toronto; and Division of Cell and Molecular Biology, Toronto General Research Institute, University Health Network, Toronto, Ontario, Canada M5G 1L7

Address all correspondence and requests for reprints to Tianru Jin: Room 10-354, Tenth Floor, Toronto Medical Discovery Tower, the MaRS Centre, University Health Network, 101 College Street, Toronto, Ontario, Canada M5G 1L7. E-mail: tianru.jin{at}utoronto.ca.

Since the relationship between TCF7L2 (also known as TCF-4) polymorphisms and type 2 diabetes mellitus was identified in 2006, extensive genome-wide association examinations in different ethnic groups have further confirmed this relationship. As a component of the bipartite transcription factor β-catenin/TCF, TCF7L2 is important in conveying Wnt signaling during embryonic development and in regulating gene expression during adulthood. Although we still do not know mechanistically how the polymorphisms within the intron regions of TCF7L2 affect the risk of type 2 diabetes, this transcriptional regulator was shown to be involved in stimulating the proliferation of pancreatic β-cells and the production of the incretin hormone glucagon-like peptide-1 in intestinal endocrine L cells. In this review, we introduce background knowledge of TCF7L2 as a component of the Wnt signaling pathway, summarize recent findings demonstrating the association between TCF7L2 polymorphisms and the risk of type 2 diabetes, outline experimental evidence of the potential function of TCF7L2 in pancreatic and intestinal endocrine cells, and present our perspective views.

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