Lactic Acid and Pyruvic Acid are byproducts of glycolysis. Carbohydrates, which contain glucose, are broken down through glycolysis to form pyruvate and two ATP molecules. Pyruvate can also be generated through the catabolism of various amino acids, including alanine, serine, cysteine, glycine, tryptophan and threonine. Magnesium is an important cofactor for a number of glycolytic enzymes necessary to produce pyruvate. Optimally, pyruvic acid is oxidized to form Acetyl-CoA to be used aerobically via the Citric Acid Cycle to produce energy. In an anaerobic state, lactic acid is formed instead.
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Low levels of pyruvic acid might imply low carbohydrate intake, lack of magnesium cofactors for glycolytic enzymes, or lack of insulin.
An elevated pyruvic acid would reflect an inability to form Acetyl-CoA to feed the Citric Acid Cycle. Pyruvate uses the pyruvate dehydrogenase complex to form Acetyl-CoA. A different enzyme, pyruvate carboxylase, is responsible for the conversion of pyruvate into oxaloacetate. Nutrient cofactors, such as vitamin-B1, B2, B3, B7, magnesium, and lipoate are needed to support the pyruvate dehydrogenase and pyruvate carboxylase enzymes.
Insufficiency in any of these nutrients can raise levels of pyruvic acid. In vitro studies have shown there are some toxins that can also affect these enzymes, such as antimony, mercury, and cadmium.
Pyruvate elevations can also be seen with a high intake of carbohydrates, as well as rare genetic forms of pyruvate dehydrogenase deficiency.
Any anerobic or low oxygen state, including pulmonary disease, anemia, sleep apnea, among others can lead to elevations of lactic acid.
Elevations of urinary lactic acid can also be the result of strenuous exercise, insulin resistance, dysglycemia, and alcohol dependence.
Zinc is an essential component in the enzymes which regulate glycolysis, such as lactate dehydrogenase (LDH). LDH converts lactate back to pyruvate in the liver via the Cori cycle. Elevations may be seen with a functional need for zinc.
Clinical Associations: Pyruvate metabolism abnormalities play important roles in cancer, heart failure, and neurodegeneration.
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