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D-2-hydroxyglutaric (DL-2-hydroxyglutaric) aciduria
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
The molecular defect in type 1 is in the activity of D-2-hydroxyglutarate dehydrogenase (see Figure 11.2) which converts D-2-hydroxyglutarate to 2-oxoglutarate. The structure of the enzyme is homologous to that of D-lactate dehydrogenase [8] and, by analogy, it is thought to transfer its electrons to electron transfer flavoprotein (ETF). The enzyme is highly active in the liver and kidney, but it is also active in the brain and heart.
Microbiology of the Vagina
Published in William J. Ledger, Steven S. Witkin, Vulvovaginal Infections, 2017
William J. Ledger, Steven S. Witkin
Lactic acid–producing bacteria are unique in their production of both the d- and l-lactic acid isomers. In contrast, mammalian cells produce l-lactic acid almost exclusively.24 The unique production of the d-lactic acid isomer by some strains of Lactobacilli may enhance protection against microbial invasion of the upper genital tract.30 Matrix metalloproteinase (MMP)-8 is known to alter the integrity of the cervix. The inducer of MMP-8, extracellular matrix metalloproteinase inducer (EMMPRIN), is produced by vaginal epithelial cells, and its concentration in vaginal secretions is dependent upon the relative levels of d- and l-lactic acid. High d-lactic acid production limits EMMPRIN concentrations, and thus MMP-8 levels and minimizes MMP-8-induced cervical changes that can promote bacterial migration to the upper genital tract. Interestingly, L. iners differs from L. crispatus, L. gasseri, and L. jensenii by its inability to produce d-lactic acid. L. iners, at least the one strain that was evaluated, was shown to lack the gene coding for d-lactate dehydrogenase.30 The clinical implications of this observation remain to be determined. However, several studies have indicated that L. iners is often associated with the presence of atypical vaginal bacteria as well as the presence of clinical symptoms.31,32 Further investigations to explore the relationship between d-lactic acid and vaginal health are warranted.
Protective effects of nanocurcumin against stress-induced deterioration in the intestine
Published in Stress, 2022
Azam Alinaghipour, Mahmoud Salami, Esmail Riahi, Ghorbangol Ashabi, Masoud Soheili, Fatemeh Nabavizadeh
Plasma D-lactate, as the end product of intestinal bacteria, has been proposed as a circulating marker to assess the extent of damage and repair of the intestinal mucosa (Fukudome et al., 2014). When the intestinal mucosa is damaged, almost all D-lactate is released into the blood due to D-lactate dehydrogenase deficiency in mammals. Therefore, D-lactate in peripheral blood can indicate damage to the intestinal barrier (Ruh et al., 2000). Our results showed that noise exposure increased the plasma D-lactate concentration. We found that nanocurcumin treatment did not reduce plasma D-lactate concentration in the stressed animals. Contrary to our finding, Xun et al. reported that curcumin reduces plasma D-lactate levels and protects the intestinal mucosal barrier function in weaned piglets challenged with enterotoxigenic Escherichia coli (Xun et al., 2015). We found that nanocurcumin reduced oxidative stress and corticosterone levels in noise-exposed rats while failing to improve intestinal integrity. Presumably, other mechanisms may be involved in altering intestinal permeability. One propose might be that nanocurcumin probably does not affect intestinal permeability in the animals exposed to noise. Although our findings are not consistent with some other research (Wang et al., 2012; Ohno et al., 2017; Tian et al., 2016), where the changes in relative protein expression of intestinal tight junctions were consistent with the plasma D-lactate level in our study. Moreover, discrepancies observed between our findings and others may be due to the different stress paradigms employed.
Host miRNA-21 promotes liver dysfunction by targeting small intestinal Lactobacillus in mice
Published in Gut Microbes, 2020
André A. Santos, Marta B. Afonso, Ricardo S. Ramiro, David Pires, Madalena Pimentel, Rui E. Castro, Cecília M.P. Rodrigues
Indeed, increasing amounts of Lactobacillus in the gut microbiota may contribute to attenuate liver disease via increased short-chain fatty acids (SCFA)30 and, in particular, via production of D-Lactate by bacteria,31 which is hydrolyzed in mammal cells by the mitochondrial D-lactate dehydrogenase (D-Ldh).32 This SCFA is an important energy substrate for liver mitochondria33 and may inhibit macrophage pro-inflammatory response.34 Although D-lactate was not detectable in serum or liver tissue, supplementation with L. reuteri induced a fourfold increase of hepatic D-Ldh mRNA. Further, increased D-lactate levels in the small intestine tissue (p = .0181) confirmed increased production in the gut (Figure 5(h)). Interestingly, in vitro experiments showed that D-lactate but not L-lactate can significantly reduce macrophage Tgf-β mRNA expression (p = .004) and protein production (p = .0124) in the absence of any inflammatory stimulus (Figure 5(i)). Thus, these results suggest that supplementation with L. reuteri and subsequent D-lactate production may protect against BDL-induced liver damaged.
Approach to the patient presenting with metabolic acidosis
Published in Acta Clinica Belgica, 2019
Jill Vanmassenhove, Norbert Lameire
D lactate acidosis occurs mostly in the setting of jejunoileal bypass or in short bowel syndrome and the standard lab test will not detect D-lactate [34]. A specific enzymatic assay using D-LDH (D-Lactate Dehydrogenase) is necessary to confirm the diagnosis. D-lactic acidosis can arise because the usual separation between GI bacteria and sugars is not adequate. D-lactic acidosis is a sign of overproduction of a variety of toxic compounds in the gastro intestinal (GI) tract that compromises central nervous system function. Classic neurological symptoms and a history of intestinal disease should raise the suspicion in a patient presenting with metabolic acidosis. D lactate is even more rapidly excreted in the urine than L lactate, the latter binding to a Na+/L-lactate cotransporter leading to tubular reabsorption. Thus also in D-lactic acidosis, the rise in the plasma AG may be lower as judged from the fall in plasma HCO3−. The plasma HCO3− might be lower than expected because of concomitant diarrhea with a load of bicarbonate loss via the stools. Treatment should be directed at the GI problem. Ingestion of fructose and complex carbohydrates should be stopped. Antacids and oral sodium bicarbonate should be avoided because these could lead to a higher intestinal pH which will increase the production of toxic products of fermentation. Drugs that lower GI motility should be stopped. Intravenous administration of sodium bicarbonate is usually not needed.