D-lactic acid metabolism after an oral load of dl-lactate

Vrese, Michael de; Koppenhoefer, Bernhard; Barth, C. A.

doi:10.1016/0261-5614(90)90069-5

Cited by 52 publications

(41 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…10 8 CFU of Lactobacillus reuterii ATCC 55730 from birth, normal blood D -lactate levels were found after 6 and 12 months, and at both time points levels were similar to the placebo group [43] . In a study in adults, de Vrese et al [20] demonstrated that after an oral D -lactate load (6 mmol/kg) the plasma level peaked at 40 min and returned to baseline 2 h later, whereas increased urinary excretion persisted for 10 h. Based on this, our results make it rather improbable that D -lactate blood concentrations were increased in the La1 group at any time.…”

Section: Discussioncontrasting

confidence: 49%

See 1 more Smart Citation

Urinary D-Lactate Excretion in Infants Receiving Lactobacillus johnsonii with Formula

et al. 2008

View full text Add to dashboard Cite

Background/Aims: Supplementation with certain probiotics can improve gut microbial flora and immune function but should not have adverse effects. This study aimed to assess the risk of D-lactate accumulation and subsequent metabolic acidosis in infants fed on formula containing Lactobacillus johnsonii (La1®). Methods: In the framework of a double-blind, randomized controlled trial enrolling 71 infants aged 4–5 months, morning urine samples were collected before and 4 weeks after being fed formulas with or without La1 (1 × 10⁸/g powder) or being breastfed. Urinary D- and L-lactate concentrations were assayed by enzymatic, fluorimetric methods and excretion was normalized per mol creatinine. Results: At baseline, no significant differences in urinary D-/L-lactate excretion among the formula-fed and breastfed groups were found. After 4 weeks, D-lactate excretion did not differ between the two formula groups, but was higher in both formula groups than in breastfed infants. In all infants receiving La1, urinary D-lactate concentrations remained within the concentration ranges of age-matched healthy infants which had been determined in an earlier study using the same analytical method. Urinary L-lactate also did not vary over time or among groups. Conclusions: Supplementation of La1 to formula did not affect urinary lactate excretion and there is no evidence of an increased risk of lactic acidosis.

show abstract

Section: Discussioncontrasting

confidence: 49%

“…The endogenous production by the methyl-glyoxylase pathway is low [17,18] , as is the renal clearance and metabolism due to lack of D -lactate-specific enzymes [19][20][21] . Thus, D -lactate found in human physiologic fluids mostly originates from external sources, i.e.…”

Section: Discussionmentioning

confidence: 99%

Urinary D-Lactate Excretion in Infants Receiving Lactobacillus johnsonii with Formula

et al. 2008

View full text Add to dashboard Cite

show abstract

“…In previous experiments, oral administration of DL-LA did not significantly influence humans physiologically or pathologically (15). This lack of effect can be explained by the much smaller amounts of DL-LA administered, a maximum of 12.8 mmol/kg 0.75 of racemic DL-LA per day.…”

Section: Discussionmentioning

confidence: 78%

d-Lactic acid-induced neurotoxicity in a calf model

Abeysekara¹,

Naylor²,

Wassef³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

Lactic acidosis (DAC) occurs as a complication of short-bowel syndrome in humans and in a variety of other gastrointestinal disorders in monogastrics and ruminants. DAC is associated with signs of impaired central nervous system (CNS) function including ataxia and coma. The objective of this experiment was to determine whether either acidification of nervous tissue or d-lactic acid is responsible for decreased neurological function. Eight Holstein calves (32 +/- 11 days, 70 +/- 10 kg) were surgically catheterized with indwelling intravenous jugular and atlanto-occipital space cerebrospinal fluid (CSF) catheters and infused for 6 h in random order with isomolar dl-lactic acid (dl-LA), l-lactic acid (l-LA), hydrochloric acid (HCl), or saline. dl-LA induced ataxia after 4 h of infusion and produced the greatest obtunding of CNS function (at 7 h, score 8.0 +/- 0.4), whereas the other infusions caused neither ataxia nor scores over 1.5 (P < 0.01 from dl-LA). dl-LA induced significantly less acidemia than HCl (at 6 h pH 7.13 +/- 0.06 and 7.00 +/- 0.04, base excess -16 +/- 1 and -23 +/- 3 mmol/l, bicarbonate 11 +/- 1 and 8 +/- 1 mmol/l respectively, all P < 0.01) but greater than l-LA and saline (P < 0.01). CSF changes followed a similar but less pronounced pattern. Although HCl infusion produced a severe acidemia and CSF acidosis, only minor effects on neurological function were evident suggesting that d-lactate has a direct neurotoxic effect that is independent of acidosis. Conversely, l-LA produced only minor neurological changes.

show abstract

“…After absorption of both isomers, only D-lactate accumulates because of its lower metabolism due to a lack of specific metabolising enzymes 7 8 and its slower renal clearance. [9][10][11] It is clear that in humans who have no D-lactic dehydrogenase, the D-2-hydroxyacid dehydrogenase that converts D-lactic acid to pyruvate in humans is likely to be responsible for metabolism. The enzyme is in high concentrations in the liver and kidney of humans and some other animals.…”

Section: Clinical Presentationsmentioning

confidence: 99%

D-lactic acidosis secondary to short bowel syndrome

Zhang

Jiang

et al. 2003

Postgraduate Medical Journal

View full text Add to dashboard Cite

A 12 year old boy presented with 11 episodes of weakness, ataxia, nausea, slurred speech, dehydration, and sometimes severe lethargy bordering on coma. A year previously the boy had small intestinal resections leaving 20 cm of small bowel remaining. D-lactic acidosis was diagnosed on the basis of a D-lactate level of 5.23 mmol/l. The clinical presentation of the disease is recurrent episodes of unusual neurological manifestations and severe metabolic acidosis. The diagnosis is dependent on the presentations and the plasma D-lactate level. Development of the syndrome seems to be the effect of the accumulation of D-lactic acid.

show abstract

D-lactic acid metabolism after an oral load of dl-lactate

Cited by 52 publications

References 24 publications

Urinary <i>D</i>-Lactate Excretion in Infants Receiving <i>Lactobacillus johnsonii</i> with Formula

Urinary <i>D</i>-Lactate Excretion in Infants Receiving <i>Lactobacillus johnsonii</i> with Formula

d-Lactic acid-induced neurotoxicity in a calf model

D-lactic acidosis secondary to short bowel syndrome

Contact Info

Product

Resources

About