期刊
CURRENT OPINION IN CLINICAL NUTRITION AND METABOLIC CARE
卷 18, 期 1, 页码 83-88出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MCO.0000000000000123
关键词
cardiovascular disease; creatine; L-homoarginine; L-arginine:glycine amidinotransferase; nitric oxide
资金
- European Union under a Marie Curie Intra-European Fellowship for Career Development
- Else Kroner-Fresenius-Stiftung
- Deutsche Forschungsgemeinschaft [CH872/1-1]
Purpose of review An increasing number of reports indicate that low levels of the endogenous amino acid L-homoarginine are linked to cardiovascular disease. In this article, we review the current findings regarding L-homoarginine metabolism and (patho-) physiology with a focus on its clinical impact. Recent findings Recent clinical and epidemiological studies revealed a strong association of low circulating L-homoarginine with cardiovascular outcomes and mortality. Human and murine studies identified L-arginine: glycine amidinotransferase (AGAT) as the responsible enzyme for endogenous L-homoarginine formation, suggesting a further important function of AGAT apart from its involvement in creatine and energy metabolism. Further studies related L-homoarginine to smoking and hypertension, and metabolic phenotypes. Summary AGAT deficiency results in diminished intracellular energy stores (i.e., ATP and phosphocreatine), as well as a lack of L-homoarginine, and has been linked to an improved metabolic risk profile, but also to impaired cardiac and cerebrovascular function. L-homoarginine's structural similarity to L-arginine suggested physiological interference with L-arginine pathways (e.g., nitric oxide). Animal experiments and clinical trials are needed to improve knowledge on the physiology of L-homoarginine and differentiate its role as marker and mediator in cardiovascular disease.
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