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Diabetes 51:3135-3138, 2002
© 2002 by the American Diabetes Association, Inc.
Brief Genetics Report |
Variations in Insulin Secretion in Carriers of the E23K Variant in the KIR6.2 Subunit of the ATP-Sensitive K+ Channel in the ß-Cell
1 Department of Molecular Cell Biology, Leiden University Medical Center, Leiden, the Netherlands
2 Department of Internal Medicine, University Medical Center, Utrecht, the Netherlands
3 Institute for Research in Extramural Medicine, VU University Medical Center, Amsterdam, the Netherlands
An association between type 2 diabetes and genetic variation in the KIR6.2 gene has been reported in several populations. Based on in vitro studies with cell lines expressing the Glu23Lys (E23K) mutation, it was recently suggested that this mutation might result in altered insulin secretion. We have examined glucose-stimulated insulin secretion in relation to this KIR6.2 gene variant in two independent Dutch cohorts. Subjects with normal (n = 65) or impaired (n = 94) glucose tolerance underwent 3-h hyperglycemic clamps at 10 mmol/l glucose. We did not observe significant differences in first- or second-phase insulin secretion between carriers and noncarriers of the gene variant in either of the study populations (all P > 0.45). Furthermore, we found no evidence for a significant interaction with disease-associated gene variants in the sulfonylurea receptor (SUR1) gene. We conclude that the E23K mutation in the KIR6.2 gene is not associated with detectable alterations in glucose-stimulated insulin secretion in two independent populations from the Netherlands.
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