An exploration of the factors that sustain glucose levels in the normal fasting subject reveals that the single major component is conservation of glucose rather than gluconeogenesis. Conservation is achieved by recycling of glucose carbon as lactate, pyruvate and alanine, and a profound decrease in the oxidation of glucose by the brain brought about by the provision and use of ketones. What glucose continues to be oxidized is for the most part formed from glycerol. Gluconeogenesis from protein plays little part in the process. Fasting hypoglycemia results from disorders affecting either one of the two critical sustaining factors--the recycling process or the availability and use of ketones. Individual hypoglycemic entities are examined against this background.