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Islet specific Wnt activation in human type II diabetes
Seung-Hee Lee1, Carla Demeterco, Ifat Geron
1Development and Aging Program, Burnham Institute for Medical Research, La Jolla, CA 92037, USA.
Experimental Diabetes Research
|January 24, 2009
Summary
Wnt signaling pathway components, including TCF7L2, are upregulated in type II diabetes. This suggests targeting Wnt signaling could be a novel therapeutic strategy for diabetes.
Area of Science:
- Endocrinology
- Molecular Biology
- Genetics
Background:
- The Wnt pathway effector gene TCF7L2 is implicated in type II diabetes.
- Understanding Wnt signaling's role in diabetes pathogenesis is crucial.
Purpose of the Study:
- To investigate the expression of Wnt pathway components in pancreatic islets of individuals with and without type II diabetes.
- To explore the potential of Wnt signaling as a therapeutic target for diabetes.
Main Methods:
- Examined Wnt pathway component expression in pancreatic tissue and isolated islets from normal and type II diabetic individuals.
- Utilized Wnt antagonist sFRP to assess the role of soluble Wnt factors in observed Wnt activation.
Main Results:
- Multiple Wnt pathway components (TCF7L2, Wnt2b, beta-catenin, pGSK3beta, TCF3, cyclinD1, c-myc) were upregulated in islets of type II diabetic patients compared to nondiabetic individuals.
- Wnt activation observed in cultured pancreatic tissue and islets was reversible by sFRP, indicating involvement of soluble Wnt factors.
Conclusions:
- The Wnt pathway plays a dynamic role in type II diabetes pathogenesis.
- Modulating Wnt signaling presents a potential new avenue for beta-cell-directed diabetes therapy.
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