Abstract
Mutations of glucokinase (GK) cause maturity-onset diabetes of the young type 2 (MODY-2), a monogenic form of diabetes that is characterized by an early age of onset and autosomal dominant inheritance. We have used a Cre/loxP strategy to generate pancreatic β-cell and hepatocyte-specific knockouts of GK in mice and have studied glucose homeostasis in these mice. The studies clearly demonstrate that diminished pancreatic β-cell GK accounts for most of the hyperglycaemia in MODY2. Mice deficient in hepatic GK are only moderately hyperglycaemic and have impaired insulin secretion. The mechanism by which the loss of hepatic GK impairs insulin secretion by the β-cell is not understood and requires further study.
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