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结肠乳酸代谢与D-乳酸酸中毒

Colonic lactate metabolism and D-lactic acidosis.

作者信息

Hove H, Mortensen P B

机构信息

Department of Medicine A, Rigshospitalet, University of Copenhagen, Denmark.

出版信息

Dig Dis Sci. 1995 Feb;40(2):320-30. doi: 10.1007/BF02065417.

Abstract

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.

摘要

D - 乳酸酸中毒见于肠道改道或短肠患者,其结肠产生的D - 乳酸会蓄积。一名患有D - 乳酸酸中毒的肠道改道患者的粪便D - 乳酸(122.4 mmol/升)和L - 乳酸(90.1 mmol/升)水平高于此前人类研究报道。血浆中D - 乳酸在数小时内波动于0.5至3.1 mmol/升之间(正常<0.1 mmol/升),尿液中波动于1.1至52.8 mmol/升之间(正常<0.7 mmol/升),这表明人体能够代谢和排泄D - 乳酸。与14名健康对照者及一名未患D - 乳酸酸中毒的肠道改道患者相比,患有D - 乳酸酸中毒的患者粪便匀浆中由葡萄糖生成的DL - 乳酸增加了10倍。富含67%碳水化合物(淀粉)的饮食使粪便和血浆乳酸略有升高,而摄入50 + 100 + 150克乳糖可使患有D - 乳酸酸中毒患者的粪便D - 乳酸(84.0 mmol/升)和血浆D - 乳酸(2.3 mmol/升)显著增加。肠道延长(回肠延长22厘米)对粪便和血浆D - 乳酸有暂时影响,但26个月后因D - 乳酸酸中毒复发(血浆8.6 mmol/升,尿液101.3 mmol/升)而恢复肠道连续性。给12名正常人大量服用乳果糖(160克/天)可使粪便中D - 乳酸增加至13.6±3.5 mmol/升,但血浆或尿液中的D - 乳酸从未增加。粪便匀浆中葡萄糖的体外发酵增加了DL - 乳酸,葡萄糖完全代谢后其消失。L - 乳酸可转化为D - 乳酸,反之亦然,二者均可降解为短链脂肪酸乙酸、丙酸和丁酸。结肠菌群产生乳酸的能力虽不常见但有所增强,可能是发生D - 乳酸酸中毒的一个先决条件,这或许可以解释为何即使在肠道改道或短肠患者中该综合征也很少见。认为D - 乳酸不被代谢因而蓄积的观点可能并不正确。

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