Abstract
Exposure to high glucose under inflammatory conditions is detrimental to insulin secreting beta cells in the pancreas. Fu and colleagues, describe a metabolic axis that reduces the production of the danger molecule nitric oxide and improves survival of beta cells exposed to an inflammatory milieu., paving the way to new interventions for diabetes.
Glucose is one of the main nutrients for the cells, and its homeostasis is finely regulated in the human body by the release of insulin by beta cells in the pancreas. Glucose greatly contributes to beta cell function and fitness1. As a consequence, the exposure to aberrant glucose levels compounded by an inflammatory milieu typical of many human diseases compromise beta cells viability, leading to the pathogenesis of diabetes2. Yet, how inflammation and glucose metabolism cooperate to regulate cell viability in these cells was until now, unclear.