Fasting-induced hypoglycemia in experimentally malnourished rats.

The ability to withstand a fasting stress as related to glucose homeostasis was studied in malnourished rats. Young male Wistar rats were fed a low-protein (D), or a low-protein, low-energy diet (M) containing, respectively, 4% protein with 70% carbohydrate (D) and 4% protein and 45% carbohydrate (M). They were compared with rats fed a control diet with 18% protein and 70% carbohydrate (C). All diets contained 8% fat. After consuming the respective diets for 4 weeks, the rats were either killed or fasted for 24 or 48 hours. Hypoglycemia developed in the malnourished rats upon fasting, but not in those receiving a complete diet. Malnourished rats had a higher blood glycine level after 4 weeks of dietary treatment. There was a marked decrease of circulating alanine and glutamate-glutamine after 48 hours of fasting in all rats. There were no differences in lysine, histidine, glycine and serine-valine. Protein malnutrition produced an increase in brain lysine, gamma-aminobutyric acid, glycine and alanine, and of glycine and alanine in liver. In contrast, D and M rats showed a depletion in muscle lysine, alanine, serine-valine and glutamate-glutamine. The fasting stress produced no changes in brain or muscle glycogen. However, liver glycogen of rats fed the D and M diets was below that of rats fed the C diet for 4 weeks. In addition, after 48 hours of fasting the C rats mobilized more exhaustively their glycogen stores that the M rats. These data suggest that in chronic malnutrition, rats may maintain their glucose homeostasis by mobilization of muscular gluconeogenic amino acids through proteolysis or de novo synthesis. Rats which were fed protein and protein-energy-deficient diets lacked adequate liver glycogen stores and their overall gluconeogenic capacity was exceeded during fasting with resultant hypoglycemia.