Comparison of the Kinetics and Utilisation of &lt;i&gt;D&lt;/i&gt;(-)- and &lt;i&gt;L&lt;/i&gt;(+)-Sodium Lactate in Normal Man

Connor, Henry; Woods, H.F.; Ledingham, J. G. G.

doi:10.1159/000176723

Cited by 65 publications

(30 citation statements)

References 8 publications

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“…A secondary role for L-LA cannot be completely excluded, as this was also infused. L-LA has been previously shown to affect D-lactic acid metabolism (11). However, our inference that D-lactate is neurotoxic is consistent with earlier work in which signs of ataxia, somnolence, and impaired palpebral reflexes developed following hypertonic sodium D-lactate injection in calves (37).…”

Section: Discussionsupporting

confidence: 91%

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d-Lactic acid-induced neurotoxicity in a calf model

Abeysekara¹,

Naylor²,

Wassef³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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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.

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Section: Discussionsupporting

confidence: 91%

“…Monocarboxylic transporters may remove D-lactate from CSF (61,62). D-Lactate in blood may be taken up by hepatic and extrahepatic tissue (13,42), although some is excreted in urine (11,17,18,32,44,63). Serum L-lactate clearance was not exponential.…”

Section: Discussionmentioning

confidence: 99%

d-Lactic acid-induced neurotoxicity in a calf model

Abeysekara¹,

Naylor²,

Wassef³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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

et al. 2008

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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.

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“…However, d ‐ α ‐Hydroxy acid dehydrogenase only metabolizes d ‐lactate at approximately one‐fifth the rate that l ‐lactate dehydrogenase metabolizes l ‐lactate (Tubbs, ; Halperin and Kamel, ). Therefore, most l ‐lactate that is generated is catabolized for energy, whereas d ‐lactate, because of its slower metabolism (Connor et al ., ), gradually accumulates in tissues.…”

Section: Introductionmentioning

confidence: 99%

Urinary d‐lactate levels reflect renal function in aristolochic acid‐induced nephropathy in mice

Huang

Chen

et al. 2013

Biomedical Chromatography

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Urinary d-lactate is highly correlated to diabetic nephropathy - a progressive kidney disease in renal glomeruli. In this study, we used a C3H/3e mouse model to investigate the relationship between urinary d-lactate and aristolochic acid nephropathy where the glomerular structure is not affected. The nephropathy was induced using intravenous injections of aristolochic acid at a dosage of 10 mg/kg per day for 5 days and was characterized biochemically and histologically. The urinary excretions of proteins, N-acetyl-β-d-glucosaminidase and serum creatinine were determined and connected to histological conventional findings. Urinary d-lactate was analyzed using column-switching high-performance liquid chromatography with fluorescence detection. The results showed a remarkable increase of urinary markers, including of urinary proteins and N-acetyl-β-d-glucosaminidase, and the histological examination confirmed a diagnosis of acute tubule necrosis. The ratio of d-lactate to creatinine in the urine of aristolochic acid-treated mice was approximately 36 times greater than that of the mice in the control group (p < 0.05). The ratios for the two groups of mice were 311.00 ± 71.70 and 8.60 ± 1.80 µmol/mmol creatinine, respectively. These data confirm in vivo that urinary d-lactate reflects renal injury conditions in aristolochic acid-treated mice and may be a marker for the assessment of nephropathy.

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Comparison of the Kinetics and Utilisation of <i>D</i>(-)- and <i>L</i>(+)-Sodium Lactate in Normal Man

Cited by 65 publications

References 8 publications

d-Lactic acid-induced neurotoxicity in a calf model

d-Lactic acid-induced neurotoxicity in a calf model

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

Urinary d‐lactate levels reflect renal function in aristolochic acid‐induced nephropathy in mice

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