The DOI matches its Crossref record; 35 of the 35 references it cites were found in a registry or an index.
The E23K Variant of Kir6.2 Associates With Impaired Post-OGTT Serum Insulin Response and Increased Risk of Type 2 Diabetes
Abstract
The E23K polymorphism of the pancreatic β-cell ATP-sensitive K+ (KATP) channel subunit Kir6.2 (KCNJ11) is associated with type 2 diabetes in whites, and a recent in vitro study of the E23K variant suggests that the association to diabetes might be explained by a slight inhibition of serum insulin release. In a study comprising 519 unrelated glucose-tolerant subjects, we addressed the question as to whether the E23K variant was related to reduced serum insulin release during an oral glucose tolerance test (OGTT). Furthermore, the polymorphism was examined in a case-control study comprising 803 type 2 diabetic patients and 862 glucose-tolerant control subjects. The E23K variant was associated with significant reductions in the insulinogenic index (P = 0.022) and serum insulin levels under the response curve during an OGTT (0–120 min) (P = 0.014) as well as with an increase in BMI (P = 0.013). In the present study, the association of the E23K polymorphism with type 2 diabetes was not significant (P = 0.26). However, the K23K genotype significantly associated with type 2 diabetes in a meta-analysis of white case and control subjects (n = 2,824, odds ratio [OR] 1.49, P = 0.00022). In conclusion, the widespread E23K polymorphism may have a diabetogenic effect by impairing glucose-induced insulin release and increasing BMI.
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Cited by
Gloyn, A. L., Pearson, E. R., Antcliff, J. F., Proks, P., Bruining, G. J., Slingerland, A. S., Howard, N., Srinivasan, S., Silva, J. M. C. L., Molnes, J., et al. (2004) · New England Journal of Medicine · doi:10.1056/nejmoa032922 · Cited by 1,137
ATP-sensitive potassium channelopathies: focus on insulin secretion
Ashcroft, F. M. (2005) · Journal of Clinical Investigation · doi:10.1172/jci25495 · Cited by 623
From pre-diabetes to diabetes: diagnosis, treatments and translational research
Khan, R., Chua, Z., Tan, J., Yang, Y., Liao, Z., & Zhao, Y. (2019) · Medicina · doi:10.3390/medicina55090546 · Cited by 484
Activating Mutations in Kir6.2 and Neonatal Diabetes
Hattersley, A. T., & Ashcroft, F. M. (2005) · Diabetes · doi:10.2337/diabetes.54.9.2503 · Cited by 414
Pancreatic β Cell Dedifferentiation in Diabetes and Redifferentiation following Insulin Therapy
Wang, Z., York, N. W., Nichols, C. G., & Remedi, M. S. (2014) · Cell Metabolism · doi:10.1016/j.cmet.2014.03.010 · Cited by 406
Metadata
- Authors
- Nielsen, E.-M. D., Hansen, L., Carstensen, B., Echwald, S. M., Drivsholm, T., Glümer, C., Thorsteinsson, B., Borch-Johnsen, K., Hansen, T., & Pedersen, O.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2003-02-01
- Volume
- 52
- Issue
- 2
- Pages
- 573-577
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2146301988
- Cited by
- 288
- References
- 35
- FWCI
- 19.43
- Type
- journal article
- Language
- en
- Open access
- closed
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- Nielsen, E.-M. D., Hansen, L., Carstensen, B., Echwald, S. M., Drivsholm, T., Glümer, C., Thorsteinsson, B., Borch-Johnsen, K., Hansen, T., & Pedersen, O. (2003). The E23K Variant of Kir6.2 Associates With Impaired Post-OGTT Serum Insulin Response and Increased Risk of Type 2 Diabetes. Diabetes. https://doi.org/10.2337/diabetes.52.2.573
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