Abstract
Overproduction of glucose is the major factor responsible for fasting hyperglycemia in type 2 diabetes. Formerly, this had been considered to be solely due to excessive hepatic glucose production because the human kidney was not regarded as an important source of glucose except during acidosis and after prolonged fasting. However, data accumulated over the last 60 years in animal and in vitro studies have provided considerable evidence that the kidney plays an important role in glucose homeostasis in conditions other than acidosis and prolonged fasting. This article summarizes early work in animals and humans, discusses methodologic issues in assessing renal glucose release in vivo, and provides evidence from recent human studies that the kidney substantially contributes to glucose overproduction in type 2 diabetes.
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