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Pharmacological effects of phosphatidylserine liposomes: regulation of gylcolysis and energy level in brain.

机译:磷脂酰丝氨酸脂质体的药理作用:调节脑中的糖酵解和能量水平。

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摘要

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.
机译:1已经通过测量糖酵解中间体和高能化合物的大脑含量,研究了通过向小鼠体内施用磷脂酰丝氨酸脂质体而产生的大脑中葡萄糖的积累。 2在正常向大脑供氧的情况下,主要在磷酸果糖激酶步骤表明抑制糖酵解。 6-磷酸葡萄糖与1,6-二磷酸果糖的比例增加,而丙酮酸,尤其是乳酸的水平降低。 3在脑缺血的情况下,磷脂酰丝氨酸的给药会延迟糖原的动员和ATP的使用。由于能量利用减少,大脑腺苷酸能电荷保持在高水平。 4结论是,磷脂酰丝氨酸诱导的脑内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所致。高水平的腺苷酸能电荷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。

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