The DOI matches its Crossref record; 39 of the 39 references it cites were found in a registry or an index.
Transcription Factor 7-Like 2 Regulates β-Cell Survival and Function in Human Pancreatic Islets
Open accessAbstract
OBJECTIVE—Type 2 diabetes is characterized by impaired insulin secretion in response to increased metabolic demand. This defect in β-cell compensation seems to result from the interplay between environmental factors and genetic predisposition. Genome-wide association studies reveal that common variants in transcription factor 7-like 2 (TCF7L2) are associated with increased risk of type 2 diabetes. The aim of the present study was to establish whether TCF7L2 plays a role in β-cell function and/or survival. RESEARCH DESIGN AND METHODS—To investigate the effects of TCFL7L2 depletion, isolated islets were exposed to TCF7L2 small interfering RNA (siRNA) versus scrambled siRNA, and β-cell survival and function were examined. For TCF7L2 overexpression, islets were cultured in glucose concentrations of 5.5–33.3 mmol/l and the cytokine mix interleukin-1β/γ-interferon with or without overexpression of TCF7L2. Subsequently, glucose-stimulated insulin secretion (GSIS), β-cell apoptosis [by transferase-mediated dUTP nick-end labeling assay and Western blotting for poly(ADP-ribose) polymerase and Caspase-3 cleavage], and β-cell proliferation (by Ki67 immunostaining) were analyzed. RESULTS—Depleting TCF7L2 by siRNA resulted in a 5.1-fold increase in β-cell apoptosis, 2.2-fold decrease in β-cell proliferation (P < 0.001), and 2.6-fold decrease in GSIS (P < 0.01) in human islets. Similarly, loss of TCF7L2 resulted in impaired β-cell function in mouse islets. In contrast, overexpression of TCF7L2 protected islets from glucose and cytokine-induced apoptosis and impaired function. CONCLUSIONS—TCF7L2 is required for maintaining GSIS and β-cell survival. Changes in the level of active TCF7L2 in β-cells from carriers of at-risk allele may be the reason for defective insulin secretion and progression of type 2 diabetes.
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2 retracted
Maedler, K., Schumann, D., Sauter, N. S., Ellingsgaard, H., Bosco, D., Baertschiger, R. M., Iwakura, Y., Oberholzer, J., Wollheim, C. B., Gauthier, B. R., et al. (2006) · Diabetes · doi:10.2337/db05-1430 · Cited by 160
Self-citationRetractedAging Correlates With Decreased β-Cell Proliferative Capacity and Enhanced Sensitivity to Apoptosis
Maedler, K., Schumann, D. M., Schulthess, F., Oberholzer, J., Bosco, D., Berney, T., & Donath, M. Y. (2006) · Diabetes · doi:10.2337/db05-1586 · Cited by 158
Self-citationRetractedβ-Cell Deficit and Increased β-Cell Apoptosis in Humans With Type 2 Diabetes
Butler, A. E., Janson, J., Bonner-Weir, S., Ritzel, R., Rizza, R. A., & Butler, P. C. (2003) · Diabetes · doi:10.2337/diabetes.52.1.102 · Cited by 4,011
A genome-wide association study of type 2 diabetes in Finns detects multiple susceptibility variants
Scott, L. J., Mohlke, K. L., Bonnycastle, L. L., Willer, C. J., Li, Y., Duren, W. L., Erdos, M. R., Stringham, H. M., Chines, P. S., Jackson, A. U., et al. (2007) · Science · doi:10.1126/science.1142382 · Cited by 2,753
Variant of transcription factor 7-like 2 (TCF7L2) gene confers risk of type 2 diabetes
Grant, S. F. A., Thorleifsson, G., Reynisdottir, I., Benediktsson, R., Manolescu, A., Sainz, J., Helgason, A., Stefansson, H., Emilsson, V., Helgadottir, A., et al. (2006) · Nature Genetics · doi:10.1038/ng1732 · Cited by 2,287
Type 2 Diabetes-a Matter of ß-Cell Life and Death?
Rhodes, C. J. (2005) · Science · doi:10.1126/science.1104345 · Cited by 896
TCF7L2 Polymorphisms and Progression to Diabetes in the Diabetes Prevention Program
Florez, J. C., Jablonski, K. A., Bayley, N., Pollin, T. I., de Bakker, P. I. W., Shuldiner, A. R., Knowler, W. C., Nathan, D. M., & Altshuler, D. (2006) · New England Journal of Medicine · doi:10.1056/nejmoa062418 · Cited by 839
Mechanisms by which common variants in the TCF7L2 gene increase risk of type 2 diabetes
Lyssenko, V., Lupi, R., Marchetti, P., Del Guerra, S., Orho-Melander, M., Almgren, P., Sjögren, M., Ling, C., Eriksson, K.-F., Lethagen, Υ.-L., et al. (2007) · Journal of Clinical Investigation · doi:10.1172/jci30706 · Cited by 829
Yi, F., Brubaker, P. L., & Jin, T. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m411487200 · Cited by 413
Saxena, R., Gianniny, L., Burtt, N. P., Lyssenko, V., Giuducci, C., Sjögren, M., Florez, J. C., Almgren, P., Isomaa, B., Orho-Melander, M., et al. (2006) · Diabetes · doi:10.2337/db06-0381 · Cited by 374
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Beta Cell Dysfunction and Insulin Resistance
Cerf, M. E. (2013) · Frontiers in Endocrinology · doi:10.3389/fendo.2013.00037 · Cited by 964
Diabetes Mellitus and the β Cell: The Last Ten Years
Ashcroft, F. M., & Rorsman, P. (2012) · Cell · doi:10.1016/j.cell.2012.02.010 · Cited by 902
The Emerging Genetic Architecture of Type 2 Diabetes
Doria, A., Patti, M.-E., & Kahn, C. R. (2008) · Cell Metabolism · doi:10.1016/j.cmet.2008.08.006 · Cited by 305
Reduced insulin exocytosis in human pancreatic β-cells with gene variants linked to type 2 diabetes
Rosengren, A. H., Braun, M., Mahdi, T., Andersson, S. A., Travers, M. E., Shigeto, M., Zhang, E., Almgren, P., Ladenvall, C., Axelsson, A. S., et al. (2012) · Diabetes · doi:10.2337/db11-1516 · Cited by 237
TCF1 links GIPR signaling to the control of beta cell function and survival
Campbell, J. E., Ussher, J. R., Mulvihill, E. E., Kolic, J., Baggio, L. L., Cao, X., Liu, Y., Lamont, B. J., Morii, T., Streutker, C. J., et al. (2016) · Nature Medicine · doi:10.1038/nm.3997 · Cited by 142
Metadata
- Authors
- Shu, L., Sauter, N. S., Schulthess, F. T., Matveyenko, A. V., Oberholzer, J., & Maedler, K.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2008-03-01
- Volume
- 57
- Issue
- 3
- Pages
- 645-653
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2161556085
- Cited by
- 265
- References
- 39
- FWCI
- 19.26
- Type
- journal article
- Language
- en
- Status
- Retracted
- Open access
- bronze
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