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Inactivating mutations in glucokinase (GCK) cause mild fasting hyperglycemia. Identification of a GCK mutation has implications for treatment and prognosis; therefore, it is important to identify these individuals. A significant number of patients have a phenotype suggesting a defect in glucokinase but no abnormality of GCK. We hypothesized that the GCK beta-cell promoter region, which currently is not routinely screened, could contain pathogenic mutations; therefore, we sequenced this region in 60 such probands.

diabetes

Identification of a Novel β-Cell Glucokinase (<i>GCK</i>) Promoter Mutation (−71G&amp;gt;C) That Modulates<i>GCK</i>Gene Expression Through Loss of Allele-Specific Sp1 Binding Causing Mild Fasting Hyperglycemia in Humans

Identification of a Novel β-Cell Glucokinase (GCK) Promoter Mutation (−71G&gt;C) That ModulatesGCKGene Expression Through Loss of Allele-Specific Sp1 Binding Causing Mild Fasting Hyperglycemia in Humans

Identification of a Novel β-Cell Glucokinase (GCK) Promoter Mutation (−71G>C) That ModulatesGCKGene Expression Through Loss of Allele-Specific Sp1 Binding Causing Mild Fasting Hyperglycemia in Humans