Bigon E, Boarato E, Bruni A, Leon A, Toffano G
Br J Pharmacol. 1979 Jun;66(2):167-74. doi: 10.1111/j.1476-5381.1979.tb13661.x.
1 The accumulation of glucose in the brain produced by the administration of phosphatidylserine liposomes into mice has been studied by measurement of the cerebral contents of glycolytic intermediates and high-energy compounds. 2 With a normal supply of oxygen to the brain, inhibition of glycolysis is indicated mainly at the phosphofructokinase step. The ratio of glucose-6-phosphate to fructose-1,6-diphosphate increased, whereas the levels of pyruvate and especially lactate decreased. 3 Under conditions of cerebral ischaemia, the administration of phosphatidylserine delays glycogen mobilization and ATP use. As a consequence of decreased energy utilization, the brain adenylate energy charge remains at a high level. 4 It is concluded that the phosphatidylserine-induced glucose accumulation in the brain is due to reduced energy expenditure and therefore to a decrease in carbohydrate consumption. The inhibition of glycolysis by the high level of adenylate energy charge is probably the control mechanism explaining the decreased carbohydrate utilization.
1 通过测量糖酵解中间产物和高能化合物的脑含量,研究了将磷脂酰丝氨酸脂质体注射到小鼠体内后大脑中葡萄糖的积累情况。2 在大脑有正常氧气供应的情况下,糖酵解的抑制主要表现在磷酸果糖激酶步骤。6-磷酸葡萄糖与1,6-二磷酸果糖的比值增加,而丙酮酸尤其是乳酸的水平降低。3 在脑缺血条件下,磷脂酰丝氨酸的给药延迟了糖原动员和ATP的使用。由于能量利用减少,脑腺苷酸能量电荷保持在高水平。4 得出的结论是,磷脂酰丝氨酸诱导的大脑中葡萄糖积累是由于能量消耗减少,因此碳水化合物消耗减少。腺苷酸能量电荷的高水平对糖酵解的抑制可能是解释碳水化合物利用减少的控制机制。