1. D-Lactic Acidosis: Pathologic Consequence of Saprophytism
Adrian Vella, M.D., Gianrico Farrugia, M.D. 
Mayo Clinic Proceedings 
Volume 73, Issue 5, Pages (May 1998)
DOI: /S (11)
Copyright © 1998 Mayo Foundation for Medical Education and Research Terms and Conditions

2. Fig. 1
Overview of pathogenesis of D-lactic acidosis. High carbohydrate load in colon creates acidic conditions favorable to overgrowth of lactobacilli and other D-lactate forming organisms. When D-lactate is absorbed in excess, such as after a large carbohydrate-rich meal, metabolism is overwhelmed, an outcome that results in episodes of acidosis and encephalopathy.
Mayo Clinic Proceedings  , DOI: ( /S (11) )
Copyright © 1998 Mayo Foundation for Medical Education and Research Terms and Conditions

3. Fig. 2
D-Lactate metabolism. Small amounts of D-lactate can be metabolized to pyruvate through D-2 hydroxyacid dehydrogenase (D-2-HDH). Acetyl CoA = acetyl coenzyme A; ATP = adenosine triphosphate; LDH = lactate dehydrogenase; PDH = pyruvate dehydrogenase; TCA = tricarboxylic acid.
Mayo Clinic Proceedings  , DOI: ( /S (11) )
Copyright © 1998 Mayo Foundation for Medical Education and Research Terms and Conditions

4. Fig. 3
D-Lactate metabolism during D-lactic acidosis. When metabolism of D-lactate through D-2-hydroxyacid dehydrogenase is overwhelmed, D-lactate enters bloodstream. High carbohydrate loads, and possibly low insulin levels, inhibit pyruvate dehydrogenase (PDH) and further increase blood levels of D-lactate. DLLR = DL-lactate racemase. For explanations of other abbreviations, see Figure 2.
Mayo Clinic Proceedings  , DOI: ( /S (11) )
Copyright © 1998 Mayo Foundation for Medical Education and Research Terms and Conditions