GK (glucokinase) catalyses the phosphorylation of glucose to glucose 6-phosphate in glucosensitive cells. In pancreatic β-cells, this reaction is the rate-limiting step of insulin release. Recent work has led to the discovery of synthetic small-molecule activators of GK that stimulate β-cell physiology and subsequently enhance the glucose-dependent release of insulin. It is currently recognized that these compounds may represent a significant advance in the development of new agents in the treatment of diabetes. In addition, GKAs (GK activators) are emerging as reagents that are useful tools with which to probe the function of pancreatic β-cells and other glucosensitive cells. This includes providing insights into the physiology of the β-cell by helping to elucidate the kinetic cycle of GK, confirming the central role of glucose metabolism to the β-cell and highlighting subtle species-dependent differences in insulin secretion between rodent and human islets of Langerhans.

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