For many years, the human kidney has been considered only to play a minimal role in glucose homeostasis. This view was mainly based on measurements of arterio-venous difference of glucose across the normal kidney after a 12-14–hour fast (basal state), indicating that very little or no glucose was released into the kidney venous blood.1 More recently, tracer-derived studies have demonstrated that this neutral kidney glucose balance is the result of a production from gluconeogenesis (˜28% of systemic glucose appearance) and simultaneous uptake (˜20% of systemic glucose disposal) (1).