L-Homoarginine is a naturally occurring, non-proteinogenic, guanidinated, cationic amino acid. It is formed in the liver in a reaction catalyzed by L-arginine:glycine amidinotransferase (AGAT) when transferring the amidino group from arginine to lysine. It is an alternative substrate for nitric oxide (NO) synthase, increases the availability of NO and thereby affects endothelial function. Homoarginine may exert further actions that are relevant to cardiovascular health, including inhibition of platelet aggregation and stimulation of insulin secretion. Recent studies demonstrate that low serum homoarginine is a strong predictor of cardiovascular mortality (2, 3, 4).
Assessment of endothelial function and cardiovascular risk.
Matrix: EDTA plasma and serum.
Volume: Minimum volume is 50 µL, but 200 µL is optimal and allows reanalysis.
Preparation and stability: The blood sample must be centrifuged and the plasma/serum fraction put on ice, and frozen.
Reported values: 1-6 µmol/L
Intraclass correlation coefficient (ICC): 0.65.
1. Midttun, O., Kvalheim, G., and Ueland, P.M. (2013). High-throughput, low-volume, multianalyte quantification of plasma metabolites related to one-carbon metabolism using HPLC-MS/MS. Anal Bioanal Chem 405, 2009-017.
2. Atzler, D., Schwedhelm, E., and Choe, C.U. (2015). L-Homoarginine and cardiovascular disease. Curr Opin Clin Nutr Metab Care 18, 83-88.
3. Tsikas, D. (2023). Homoarginine in health and disease. Curr Opin Clin Nutr Metab Care 26, 42-49.
4. Koch, V., Gruenewald, L. D., Gruber-Rouh, T., Eichler, K., Leistner, D. M., Mahmoudi, S., Booz, C., Bernatz, S., D’Angelo, T., et al. (2022). Homoarginine in the cardiovascular system: Pathophysiology and recent developments. Fundam Clin Pharmacol 37, 519-529.