Bhattacharya S B, Datta A G
Indian Institute of Chemical Biology, Calcutta.
Mol Cell Biochem. 1993 Aug 11;125(1):51-7. doi: 10.1007/BF00926834.
Glucagon increased the activities of alanine amino transferase (AAT), fructose-1:6-bisphosphatase (fru-P2ase) and glucose-6-phosphatase (G-6-Pase) in goat brain tissue by about 100%, 150% and 50% respectively. These increase in activities were reversed by beta-antagonists propranolol. Well known alpha-agonist and antagonist like phenylephrine and phenoxybenzamine also increased AAT and G-6-Pase activities and these increased activities were reversed by propranolol. Phenylephrine and phenoxybenzamine however did not increase brain Fru-P2ase activity. However the most interesting finding is that cerebral cortical slices could produce glucose from alanine and this glucose production was enhanced by glucagon, phenylephrine and phenoxybenzamine. Propranolol reversed the effects of these agonists and antagonist to a great extent. From all these experiments we suggest brain to be a gluconeogenic organ although much less efficient than liver.
胰高血糖素使山羊脑组织中丙氨酸氨基转移酶（AAT）、果糖-1:6-二磷酸酶（fru-P2ase）和葡萄糖-6-磷酸酶（G-6-Pase）的活性分别增加了约100%、150%和50%。β受体拮抗剂普萘洛尔可逆转这些活性的增加。苯肾上腺素和酚苄明等知名的α受体激动剂和拮抗剂也增加了AAT和G-6-Pase的活性，而普萘洛尔可逆转这些增加的活性。然而，苯肾上腺素和酚苄明并未增加脑内fru-P2ase的活性。然而，最有趣的发现是大脑皮质切片能够从丙氨酸生成葡萄糖，且胰高血糖素、苯肾上腺素和酚苄明可增强这种葡萄糖生成。普萘洛尔在很大程度上逆转了这些激动剂和拮抗剂的作用。从所有这些实验中我们认为，大脑是一个糖异生器官，尽管其效率远低于肝脏。
