Glucokinase catalyzes a rate-limiting step in glucose metabolism in hepatocytes and pancreatic beta cells and is considered the "glucose sensor" for regulation of insulin secretion. Patients with maturity-onset diabetes of the young (MODY) have heterozygous point mutations in the glucokinase gene that result in reduced enzymatic activity and decreased insulin secretion. Disruption of the glucokinase gene results in a phenotype similar to MODY in heterozygous mice. These mice manifest a decreased insulin secretory response to glucose.

These <i> Gck</i> knock-out mice exhibit a decreased insulin secretory response to glucose. They are suitable for use in applications related to the study of maturity-onset diabetes.

Typically mice are recovered in 12-16 weeks. Contact Customer Service to place an order or for more information.

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