COLONIC LACTATE METABOLISM AND D-LACTIC ACIDOSIS
COLONIC LACTATE METABOLISM AND D-LACTIC ACIDOSIS
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DOI：
10.1007/bf02065417
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发表时间：
1995-02-01
影响因子：
3.1
通讯作者：
MORTENSEN, PB
中科院分区：
文献类型：
--
作者：
HOVE, H;MORTENSEN, PB
D-乳酸酸中毒见于肠旁路或短肠患者，其中结肠产生的D-乳酸蓄积。一位患有D-乳酸酸中毒的肠道旁路患者的粪便D-乳酸（122.4 mmol/L）和L-乳酸（90.1 mmol/L）高于之前在人类中的描述。在几小时内，血浆中D-乳酸盐在0.5和3.1 mmol/L之间波动（正常< 0.1 mmol/L），尿液中D-乳酸盐在1.1和52.8 mmol/L之间波动（正常< 0.7 mmol/L），表明人体生物体确实代谢和排泄D-乳酸盐。与14名健康对照组和1名没有D-乳酸酸中毒的肠旁路患者相比，D-乳酸酸中毒患者粪便匀浆中葡萄糖产生的DL-乳酸增加了10倍。富含67%碳水化合物（淀粉）的饮食导致粪便和血浆乳酸盐轻微升高，而50 + 100 + 150 g摄入的乳糖显著增加了D-乳酸酸中毒患者粪便（84.0 mmol/L）和血浆（2.3 mmol/L）中的D-乳酸盐。肠道延长（22 cm回肠）对粪便和血浆D-乳酸有暂时影响，但26个月后由于D-乳酸酸中毒复发（血浆8.6 mmol/L，尿液101.3 mmol/L），肠道连续性得以重建。对12名正常人给予大量乳果糖（160 g/天）可使粪便中的D-乳酸增加至13.6 +/- 3.5 mmol/L，但从未增加血浆或尿液中的D-乳酸。粪便匀浆中葡萄糖的体外发酵增加DL-乳酸，其在葡萄糖完全代谢后消失。L-乳酸盐转化为D-乳酸盐，反之亦然，两者都降解为短链脂肪酸乙酸盐、丙酸盐和丁酸盐。结肠植物群产生乳酸的能力虽不常见，但却升高，这可能是D-乳酸酸中毒发生的先决条件，也可能解释了为什么即使在肠旁路或短肠患者中也很少见到该综合征。D-乳酸盐不被代谢并因此蓄积的建议可能是不正确的。
D-Lactic acidosis is seen in patients with intestinal bypass or short bowels in whom colonic produced D-lactate accumulates. An intestinal bypassed patient with D-lactic acidosis had higher fecal D-lactate (122.4 mmol/liter) and L-lactate (90.1 mmol/liter) than described before in humans. D-Lactate fluctuated between 0.5 and 3.1 mmol/liter in plasma (normal < 0.1 mmol/liter) and between 1.1 and 52.8 mmol/liter in urine (normal < 0.7 mmol/liter) within a few hours, indicating that the human organism do metabolize and excrete D-lactate. The patient with D-lactic acidosis had a 10-fold increased DL-lactate production from glucose in fecal homogenates compared to 14 healthy controls and a patient with intestinal bypass, who did not have D-lactic acidosis. A 67% carbohydrate (starch)-enriched diet resulted in a minor elevation of fecal and plasma lactate, whereas 50 + 100 + 150 g of ingested lactose increased D-lactate in feces (84.0 mmol/liter) and plasma (2.3 mmol/liter) considerably in the patient with D-lactic acidosis. Intestinal prolongation (22 cm ileum) had a temporary effect on fecal and plasma D-lactate, but intestinal continuity was reestablished 26 months later because D-lactic acidosis recurred (plasma 8.6 mmol/liter, urine 101.3 mmol/liter). Large amounts of lactulose (160 g/day) to 12 normal individuals increased D-lactate to 13.6 +/- 3.5 mmol/liter in feces, but never increased D-lactate in plasma or urine. The in vitro fermentation of glucose in fecal homogenates increased DL-lactate, which disappeared after complete metabolization of the glucose. L-Lactate was converted to D-lactate and vice versa, and both were degraded to the short-chain fatty acids acetate, propionate, and butyrate. An infrequent, but elevated ability of the colonic flora to produce lactate may be a prerequisite for D-lactic acidosis to occur and may explain why the syndrome is so seldom seen even in patients with intestinal bypass or short bowels. The suggestion that D-lactate is not metabolized and hence accumulates is probably not valid.