1222 ALTERED CEREBRAL SUBSTRATE UTILIZATION BY THE HYPOGLYCEMIC DOG

Abstract

Insulin infusion to 3 hr old term dogs (n=6, control=6)lowered blood glucose (1.31±0.17 vs 8.12±0.29 mM p<0.001) and lactate (1.05±0.13 vs 1.72±0.22 p<0.01), without altering clinical behavior. Freeze clamped cerebral cortex (<3sec) revealed reduced glycogen content (1.35±0.25 vs 1.98±0.20 umol/g p<0.05) and glucose 6-phosphate levels (0.068±0.013 vs 0.115±0.021 p<0.02) following hypoglycemia. Cerebral phosphoenolpyruvate and pyruvate levels were augmented during hypoglycemia while cerebral cortical lactate was diminished (0.774±0.054 vs 1.40±0.15 p<0.01). Furthermore, citrate (0.210±0.004 vs 0.353±0.009 p<0.001) and malate levels (0.103±0.016 vs 0.197±0.022 p<0.01) were diminished during hypoglycemia while alpha ketoglutarate was not altered. Cerebral amino acids, aspartate and glutamate were unchanged. However, alanine (0.477±0.041 vs 0.680±0.080 p<0.05) and glutamine (6.24 ±0.40 vs 7.68±0.06 p<0.01) were reduced during hypoglycemia. In addition, during hypoglycemia cerebral ammonia levels were elevated (1.12±0.24 vs 0.58±0.02 p<0.02). Nonetheless, cerebral ATP levels were not affected. These data suggest that neonatal cerebral energy status was not altered by diminished circulating levels of oxidizable cerebral substrates, glucose and lactate. The small pool of cerebral glycogen may be mobilized to contribute to energy production. Nonetheless, the much larger pool of cerebral amino acids via transamination and deamination reactions may become a more important source for cerebral energy production during hypoglycemia than during euglycemia.

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