D-Lactate is normally present in the blood of mammals at nanomolar concentrations due to methylglyoxal metabolism; millimolar D-lactate concentrations can arise due to excess gastrointestinal microbial production. Grain overload in ruminants, short-bowel syndrome in humans, and diarrhea in calves can all result in profound D-lactic acidemia, with remarkably similar neurological manifestations. In the past, D-lactate was thought to be excreted mainly in the urine, and metabolized slowly by the enzyme D-α-hydroxy acid dehydrogenase. More recent studies reported that mammals have a relatively high capacity for D-lactate metabolism and identified a putative: mammalian D-lactate dehydrogenase. A growing body of literature is also emerging describing subclinical elevation of D-lactate as an indicator of sepsis and trauma. This article describes advances in the understanding of D-lactate metabolism, D-lactic acidosis in ruminants and humans, and subclinical elevation of D-lactate. © 2005 American Society for Nutritional Sciences.
CITATION STYLE
Ewaschuk, J. B., Naylor, J. M., & Zello, G. A. (2005). D-lactate in human and ruminant metabolism. Journal of Nutrition. American Institute of Nutrition. https://doi.org/10.1093/jn/135.7.1619
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