The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Both Maximal Expression of Selenoproteins and Selenoprotein Deficiency Can Promote Development of Type 2 Diabetes-Like Phenotype in Mice
Open accessAbstract
Selenium (Se) is an essential trace element in mammals that has been shown to exert its function through selenoproteins. Whereas optimal levels of Se in the diet have important health benefits, a recent clinical trial has suggested that supplemental intake of Se above the adequate level potentially may raise the risk of type 2 diabetes mellitus. However, the molecular mechanisms for the effect of dietary Se on the development of this disease are not understood. In the present study, we examined the contribution of selenoproteins to increased risk of developing diabetes using animal models. C57BL/6J mice (n=6-7 per group) were fed either Se-deficient Torula yeast-based diet or diets supplemented with 0.1 and 0.4 parts per million Se. Our data show that mice maintained on an Se-supplemented diet develop hyperinsulinemia and have decreased insulin sensitivity. These effects are accompanied by elevated expression of a selective group of selenoproteins. We also observed that reduced synthesis of these selenoproteins caused by overexpression of an i(6)A(-) mutant selenocysteine tRNA promotes glucose intolerance and leads to a diabetes-like phenotype. These findings indicate that both high expression of selenoproteins and selenoprotein deficiency may dysregulate glucose homeostasis and suggest a role for selenoproteins in development of diabetes.
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Cites
Targeted disruption of the chop gene delays endoplasmic reticulum stress-mediated diabetes
Oyadomari, S., Koizumi, A., Takeda, K., Gotoh, T., Akira, S., Araki, E., & Mori, M. (2002) · Journal of Clinical Investigation · doi:10.1172/jci0214550 · Cited by 752
Reactive oxygen species enhance insulin sensitivity
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Development of insulin resistance and obesity in mice overexpressing cellular glutathione peroxidase
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Self-citationHandy, D. E., Lubos, E., Yang, Y., Galbraith, J. D., Kelly, N., Zhang, Y.-Y., Leopold, J. A., & Loscalzo, J. (2009) · Journal of Biological Chemistry · doi:10.1074/jbc.m900392200 · Cited by 187
Self-citationMoustafa, M. E., Carlson, B. A., El-Saadani, M. A., Kryukov, G. V., Sun, Q.-A., Harney, J. W., Hill, K. E., Combs, G. F., Feigenbaum, L., Mansur, D. B., et al. (2001) · Molecular and Cellular Biology · doi:10.1128/mcb.21.11.3840-3852.2001 · Cited by 131
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Cited by
Rayman, M. P. (2012) · The Lancet · doi:10.1016/s0140-6736(11)61452-9 · Cited by 3,563
Paradoxical Roles of Antioxidant Enzymes: Basic Mechanisms and Health Implications
Lei, X. G., Zhu, J.-H., Cheng, W.-H., Bao, Y., Ho, Y.-S., Reddi, A. R., Holmgren, A., & Arnér, E. S. J. (2016) · Physiological Reviews · doi:10.1152/physrev.00010.2014 · Cited by 429
Selenium exposure and the risk of type 2 diabetes: A systematic review and meta-analysis
Vinceti, M., Filippini, T., & Rothman, K. J. (2018) · European Journal of Epidemiology · doi:10.1007/s10654-018-0422-8 · Cited by 233
Yang, S. J., Hwang, S. Y., Choi, H. Y., Yoo, H. J., Seo, J. A., Kim, S. G., Kim, N. H., Baik, S. H., Choi, D. S., & Choi, K. M. (2011) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2011-0620 · Cited by 191
Wu, R. T., Cao, L., Mattson, E., Witwer, K. W., Cao, J., Zeng, H., He, X., Combs, G. F., & Cheng, W. (2017) · Aging Cell · doi:10.1111/acel.12529 · Cited by 37
Metadata
- Authors
- Labunskyy, V. M., Lee, B. C., Handy, D. E., Loscalzo, J., Hatfield, D. L., & Gladyshev, V. N.
- Venue
- Antioxidants & Redox Signaling
- Publisher
- SAGE Publications
- Published
- 2011-06-15
- Volume
- 14
- Issue
- 12
- Pages
- 2327-2336
- ISSN
- 1523-0864 (ISSN-L)
- 1557-7716
- OpenAlex
- W2007135892
- Cited by
- 189
- References
- 6
- FWCI
- 11.52
- Type
- journal article
- Language
- en
- Open access
- green
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- Labunskyy, V. M., Lee, B. C., Handy, D. E., Loscalzo, J., Hatfield, D. L., & Gladyshev, V. N. (2011). Both Maximal Expression of Selenoproteins and Selenoprotein Deficiency Can Promote Development of Type 2 Diabetes-Like Phenotype in Mice. Antioxidants & Redox Signaling. https://doi.org/10.1089/ars.2010.3526
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