Lactic Acid

Sample type: Urine
Optimal result: 0 – 23.08 ug/mg CR

Dietary carbohydrates are broken down into glucose and other sugars where carbohydrate breakdown products, pyruvic acid and lactic acid are formed. Pyruvic acid enters the krebs cycle via dehydrogenase enzymes which require vitamin B1 (thiamine), vitamin B2 (riboflavin), vitamin B3 (niacin), vitamin B5 (pantothenic acid) and lipoic acid to function correctly.

In the absence of these nutrients, lactic acid builds up leading to lactic acidosis. Elevated pyruvic acid and lactic acid can indicate a need for lipoic acid.

- Elevated Lactic acid is associated with vigorous exercise, bacterial overgrowth, shock, B-vitamin deficiency, inborn errors of metabolism and anemia.

- Elevated Lactic acid inborn errors of metabolism may include disorders of sugar metabolism, pyruvate dehydrogenase deficiency and mitochondrial disorders.

Consider: Vitamin B1 (thiamine), vitamin B2 (riboflavin), vitamin B3 (niacin), vitamin B5 (pantothenic acid), lipoic acid and coenzyme Q10.

Low levels of pyruvic acid might imply low carbohydrate intake, lack of magnesium cofactors for glycolytic enzymes, or lack of insulin.

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.

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.

References:

- Pieczenik SR, Neustadt J. Mitochondrial dysfunction and molecular pathways of disease. Exp Mol Pathol. 2007 Aug;83(1):84-92. doi: 10.1016/j.yexmp.2006.09.008. Epub 2007 Jan 18. PMID: 17239370.

- Depeint F, Bruce WR, Shangari N, Mehta R, O'Brien PJ. Mitochondrial function and toxicity: role of the B vitamin family on mitochondrial energy metabolism. Chemico-biol Interact. 2006;163(1-2):94-112.

- Gray LR, Tompkins SC, Taylor EB. Regulation of pyruvate metabolism and human disease. Cell Mol Life Sci. 2014;71(14):2577-2604.

- Garfinkel L, Garfinkel D. Magnesium regulation of the glycolytic pathway and the enzymes involved. Magnesium. 1985;4(2-3):60- 72.

- Mayes PA, Bender DA. Glycolysis and the oxidation of pyruvate. Harper’s illustrated biochemistry (Eds RK Murray, DK Granner, PA Mayes, VW Rodwell) pp. 2003:136-144.

- Ravindran S, Radke GA, Guest JR, Roche TE. Lipoyl domainbased mechanism for the integrated feedback control of the pyruvate dehydrogenase complex by enhancement of pyruvate dehydrogenase kinase activity. J Biol Chem. 1996;271(2):653-662.

- Shipman K. Clinical biochemistry: Metabolic and clinical aspects (3rd edn). In: SAGE Publications Sage UK; 2015.

- Tirmenstein MA, Mathias PI, Snawder JE, Wey HE, Toraason M. Antimony-induced alterations in thiol homeostasis and adenine nucleotide status in cultured cardiac myocytes. Toxicology. 1997;119(3):203-211.

- Chapatwala KD, Rajanna B, Desaiah D. Cadmium induced changes in gluconeogenic enzymes in rat kidney and liver. Drug Chem Toxicol. 1980;3(4):407-420.

- Schlecht I, Gronwald W, Behrens G, et al. Visceral adipose tissue but not subcutaneous adipose tissue is associated with urine and serum metabolites. PloS one. 2017;12(4):e0175133.

- Friedrich N, Skaaby T, Pietzner M, et al. Identification of urine metabolites associated with 5-year changes in biomarkers of glucose homoeostasis. Diab Metab. 2017.

- Mostafa H, Amin AM, Teh CH, Murugaiyah V, Arif NH, Ibrahim B. Metabolic phenotyping of urine for discriminating alcoholdependent from social drinkers and alcohol-naive subjects. Drug Alc Depend. 2016;169:80-84.

- Hira HS, Shukla A, Kaur A, Kapoor S. Serum uric acid and lactate levels among patients with obstructive sleep apnea syndrome: which is a better marker of hypoxemia? Ann Saudi Med. 2012;32(1):37-42.

- Nikolaidis S, Kosmidis I, Sougioultzis M, Kabasakalis A, Mougios V. Diurnal variation and reliability of the urine lactate concentration after maximal exercise. Chronobiol Int. 2018;35(1):24-34.

- Tamaki N, Ikeda T, Funatsuka A. Zinc as activating cation for muscle glycolysis. J Nutr Sci Vitaminol. 1983;29(6):655-662.

- Ikeda T, Kimura K, Morioka S, Tamaki N. Inhibitory effects of Zn2+ on muscle glycolysis and their reversal by histidine. J Nutr Sci Vitaminol. 1980;26(4):357-366.

- Kaplan RS, Mayor JA, Blackwell R, Maughon RH, Wilson GL. The effect of insulin supplementation on diabetes-induced alterations in the extractable levels of functional mitochondrial anion transport proteins. Arch Biochem Biophys. 1991;287(2):305-311.

Lactic Acid
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