A balance of glucose uptake and secretion are important for life. Glucose if the main fuel for the brain and red blood cells. When an organism is not feeding (that is, when the individual is fasting) the body needs to be able to synthesize glucose from glycogen or other non-carbohydrate sources. F 1,6-BPase is essential to the conversion of these reserves to glucose. The inhibition of F 1,6-BPase in mammals results in reduced levels of serum glucose in the fasting state. Hence, F 1,6-BPase is a target for the development of drugs in the treatment of non-insulin dependent diabetes, which afflicts over 15 million people in the United States (7).      Inheritance of F 1,6-BPase deficiency is autosomal recessive. The incidence is unknown. The disorder results in fasting hypoglycemia, ketosis, and acidosis and can be fatal in newborns. Febrile illness can trigger later episodes. The enzymatic block leads to accumulation of gluconeogenic precursors--certain amino acids, lactic acid, and ketoacids. Symptoms can be relieved by oral glucose, or IV glucose if hypoglycemia is severe. Tolerance to fasting generally improves with age (9).