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Studies of the Impact of a Liver Glucokinase Promoter Variant on Glucose Tolerance and Insulin Sensitivity Index¹

Steno Diabetes Center and Hagedorn Research Institute (S.A.U., T.H., L.B.J., L.H., O.P.), Copenhagen, Denmark; Center of Preventive Medicine (J.C.), Glostrup University Hospital, Copenhagen, Denmark; and Division of Endocrinology and Metabolism (K.C.C.), University of California Los Angeles School of Medicine, Los Angeles, California

Address all correspondence and requests for reprints to: Søren A. Urhammer, M.D., Steno Diabetes Center, Niels Steensens Vej 2, DK-2820 Gentofte, Denmark. E-mail: sau{at}novo.dk

Because a frequently occurring nucleotide substitution at position -258 in the liver glucokinase promoter has been reported to be associated with impaired promoter activity, we have examined in Danish Caucasians whether this variant is associated with alterations in glucose tolerance and/or the insulin sensitivity index (Si). Among 246 Danish Caucasian patients with noninsulin-dependent diabetes mellitus, the allelic frequency of the -258 promoter variant was 15.2% (95% confidence interval: 12.0–18.4%) vs. 16.5% (13.2–19.8%) among 242 matched control subjects. In the control group, the glucokinase variant was not related to serum insulin or plasma glucose levels before or during an oral glucose tolerance test. Neither was the gene variant among 380 young, healthy subjects associated with altered Si or altered insulin secretion after an iv glucose load. We conclude that in Danish Caucasians, the -258 glucokinase promoter variant has no impact on glucose tolerance, whole-body Si, or insulin secretion.

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