Sadeghi-Nejad A, Hochman H, Senior B
J Pediatr. 1975 Jan;86(1):37-42. doi: 10.1016/s0022-3476(75)80701-3.
Paradoxically, ethanol, which raises lactate in normal individuals, lowers the elevated levels of lactate in patients with Type I glycogenosis. We found that, although lactate levels fell, pyruvate proportionately declined even more, resulting in an increased L/P ratio which indicates that, as in the normal, the oxidation of ethanol had generated NADH. In type I glycogenosis, the increased level of pyruvate-lactate derives from glycogenolysis. We found that, despite continued glycogenolysis, ethanol had caused less pyruvate-lactate to form. The effect of an increased NADH/NAD+ ratio on the flow of carbon through the Embden-Meyerhof pathway could account for the finding, presumably by its effect on the oxidation-reduction couples with diversion of carbon toward formation of triglyceride rather than pyruvate-lactate.
矛盾的是，乙醇在正常个体中会升高乳酸水平，但却能降低I型糖原贮积症患者升高的乳酸水平。我们发现，虽然乳酸水平下降，但丙酮酸相应地下降得更多，导致L/P比值升高，这表明与正常情况一样，乙醇的氧化产生了NADH。在I型糖原贮积症中，丙酮酸-乳酸水平升高源于糖原分解。我们发现，尽管糖原分解持续进行，但乙醇使丙酮酸-乳酸的形成减少。NADH/NAD+比值增加对通过糖酵解途径的碳流的影响可以解释这一发现，推测是通过其对氧化还原偶联的影响，使碳转向甘油三酯的形成而非丙酮酸-乳酸的形成。
