Recent decades have seen an incredible growth in the prevalence of diabetes. While it is important to pursue multiple therapeutic strategies, harnessing the regenerative capacity of islet β-cells to increase an individual’s insulin secretion capacity is among the promising approaches.

Recently, discovery-oriented unbiased chemical screening led to the identification of the metabolic enzyme adenosine kinase (ADK) as a regulator of rodent and porcine β-cell replication. Importantly, small molecule ADK-inhibitors selectively stimulate replication of β-cells, but not alpha-cells, in vitro and in vivo. The identification of ADK as a regulator of β-cell regeneration has raised several important questions.

Does long-term inhibition of ADK in vivo promote β-cell mass expansion and protect against developing diabetes? How does a broadly expressed metabolic enzyme selectively control the growth of a specific cell-type?

Is human β-cell growth controlled by ADK? Using the nPOD resources, we are investigating the expression of ADK in normal and diabetic pancreatic tissues. We are interested in weather this molecule is expressed in human β-cells and whether its expression changes with diseased states.