Abstract
In contrast to L-lactate, D-lactate is produced in minimal quantities by human cells, and the plasma D-lactate concentration normally is maintained at a concentration of only about 0.01 mM. However, in short bowel syndrome, colonic bacterial production of D-lactate may lead to plasma concentrations >3mM with accompanying acidosis and neurological symptoms – a syndrome known as D-lactic acidosis. Minor increases in plasma D-lactate have been observed in various gastrointestinal conditions such as ischemia, appendicitis and Crohn’s disease, a finding touted to have diagnostic utility. The novel aspect of this review paper is the application of numerical values to the processes involved in D-lactate homeostasis that previously have been described only in qualitative terms. This approach provides a number of new insights into normal and disordered production, catabolism and excretion of D-lactate, and identifies multiple gaps in our understanding of D-lactate physiology that should be amenable to relatively simple investigative study.
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