ABSTRACT
Glucose is an obligate fuel for the brain under physiologic conditions [1]. Indeed, glucose homeostasis is maintained by one hormone (insulin), which lowers glucose, and counter-regulatory mediators (glucagon, catecholamines, cortisol, and growth hormone), which raise glucose concentrations and facilitate the transition to the use of lipid-derived substrates during prolonged fasting. In such circumstances, glucose may be lower than typical fasting values, but because of appropriate metabolic and counter-regulatory changes, cognition is not impaired and no symptoms of neuroglycopenia are apparent. As such, establishing a diagnosis of a hypoglycemic disorder requires the documentation of Whipple’s triad [2]; namely, a low plasma glucose concentration (≤55–60 mg/dL) must be measured with a precise method at the time of symptoms consistent with hypoglycemia, and these symptoms must be relieved by correction of the hypoglycemia. Only after these criteria are fulfilled should one embark on testing the mechanism by which hypoglycemia occurs [3].
