EFFECTS OF UNBALANCED DIETS ON CEREBRAL GLUCOSE-METABOLISM IN THE ADULT-RAT

We measured regional cerebral metabolic rates for glucose and selected cerebral metabolites in rats fed one of the following diets for 6 to 7 weeks: (1) regular laboratory chow; (2) high-fat, carbohydrate-free ketogenic diet deriving 10% of its caloric value from proteins and 90% from fat; and (3) high-carbohydrate diet deriving 10% of its caloric value from proteins, 78% from carbohydrates, and 12% from fat. In prel iminary experiments, we found that moderate ketosis could not be achie ved by diets deriving less than about 90% of their caloric value from fat. Rats maintained on the ketogenic diet had moderately elevated blo od beta-hydroxybutyrate (0.4 mM) and acetoacetate (0.2 mM), and a five - to 10-fold increase in their cerebral beta-hydroxybutyrate level. Ce rebral levels of glucose, glycogen, lactate, and citrate were similar in all groups. 2-Deoxyglucose studies showed that the ketogenic diet d id not significantly alter regional brain glucose utilization. However , rats maintained on the high-carbohydrate diet had a marked decrease in their brain glucose utilization and increased cerebral concentratio ns of glucose 6-phosphate. These findings indicate that long-term mode rate ketonemia does not significantly alter brain glucose phosphorylat ion. However, even marginal protein dietary deficiency, when coupled w ith a carbohydrate-rich diet, depresses cerebral glucose utilization t o a degree often seen in metabolic encephalopathies. Our results suppo rt the clinical contention that protein dietary deficiency coupled wit h increased carbohydrate intake can lead to CNS dysfunction.