L-Arginine

Biochem Biophys Res Commun. 2014 Nov 7;454(1):53-7.

Oral supplementation with a combination of L-citrulline and L-arginine rapidly increases plasma L-arginine concentration and enhances NO bioavailability.[Pubmed: 25445598]

Chronic supplementation with L-citrulline plus L-Arginine has been shown to exhibit anti-atherosclerotic effects. However, the short-term action of this combination on the nitric oxide (NO)-cGMP pathway remains to be elucidated. The objective of the present study was to investigate the acute effects of a combination of oral L-citrulline and L-Arginine on plasma L-Arginine and NO levels, as well as on blood circulation.
METHODS AND RESULTS:
Rats or New Zealand white rabbits were treated orally with L-citrulline, or L-Arginine, or a combination of each at half dosage. Following supplementation, plasma levels of L-Arginine, NOx, cGMP and changes in blood circulation were determined sequentially. L-Citrulline plus L-Arginine supplementation caused a more rapid increase in plasma L-Arginine levels and marked enhancement of NO bioavailability, including plasma cGMP concentrations, than with dosage with the single amino acids. Blood flow in the central ear artery in rabbits was also significantly increased by L-citrulline plus L-Arginine administration as compared with the control.
CONCLUSIONS:
Our data show for the first time that a combination of oral L-citrulline and L-Arginine effectively and rapidly augments NO-dependent responses at the acute stage.

Immunology. 2014 Oct;143(2):184-92.

L-Arginine modulates neonatal lymphocyte proliferation through an interleukin-2 independent pathway.[Pubmed: 24697328 ]

In cases of arginine depletion, lymphocyte proliferation, cytokine production and CD3ζ chain expression are all diminished. In addition to myeloid suppressor cells, polymorphonuclear cells (PMN) also exert T-cell immune suppressive effects through arginase-induced L-Arginine depletion, especially during pregnancy.
METHODS AND RESULTS:
In this study, we investigated how arginase/L-Arginine modulates neonatal lymphocyte proliferation. Results showed that the neonatal plasma L-Arginine level was lower than in adults (48·1 ± 11·3 versus 86·5 ± 14·6 μm; P = 0·003). Neonatal PMN had a greater abundance of arginase I protein than adult PMN. Both transcriptional regulation and post-transcriptional regulation were responsible for the higher arginase I expression of neonatal PMN. Exogenous L-Arginine enhanced neonate lymphocyte proliferation but not that of adult cells. The RNA-binding protein HuR was important but was not the only modulation factor in L-Arginine-regulated neonatal T-cell proliferation. L-Arginine-mediated neonatal lymphocyte proliferation could not be blocked by interleukin-2 receptor blocking antibodies.
CONCLUSIONS:
These results suggest that the altered arginase/L-Arginine cascade may be one of the mechanisms that contribute to altered neonatal immune responses. Exogenous L-Arginine could enhance neonate lymphocyte proliferation through an interleukin-2-independent pathway.

Amino Acids. 2014 Oct;46(10):2271-86.

L-Arginine and its metabolites in kidney and cardiovascular disease.[Pubmed: 25161088]

L-Arginine is a semi essential amino acid synthesised from glutamine, glutamate and proline via the intestinal-renal axis in humans and most mammals. L-Arginine degradation occurs via multiple pathways initiated by arginase, nitric-oxide synthase, Arg: glycine amidinotransferase, and Arg decarboxylase. These pathways produce nitric oxide, polyamines, proline, glutamate, creatine and agmatine with each having enormous biological importance. Several disease are associated to an L-Arginine impaired levels and/or to its metabolites: in particular various L-Arginine metabolites may participate in pathogenesis of kidney and cardiovascular disease. L-Arginine and its metabolites may constitute both a marker of pathology progression both the rationale for manipulating L-Arginine metabolism as a strategy to ameliorate these disease. A large number of studies have been performed in experimental models of kidney disease with sometimes conflicting results, which underlie the complexity of Arg metabolism and our incomplete knowledge of all the mechanisms involved.
CONCLUSIONS:
This review will discuss the implication of the mains L-Arginine metabolites and L-Arginine-derived guanidine compounds in kidney and cardiovascular disease considering the more recent literature in the field.

Chem Biol Interact. 2015 Mar 5;229:9-16.

Modulatory effects of l-arginine and soy enriched diet on bone homeostasis abnormalities in streptozotocin-induced diabetic rats.[Pubmed: 25617479]

Diabetes mellitus is a complex syndrome which is responsible for numerous complications affecting the whole body. Osteoporosis is regarded as one of the chronic complications of diabetes mellitus that results from reduced bone formation and increased resorption.
METHODS AND RESULTS:
In this context, we searched for dietary supplements that preserve diabetic bone loss. Parathyroid hormone (PTH) has been suggested as a possible mechanism affecting bone homeostasis in streptozotocin (STZ)-induced diabetic rats. The osteoprotective effects of L-Arginine and soy enriched diet were also investigated. Male Wistar rats were allocated into four groups; normal control, untreated STZ-diabetic rats and STZ-diabetic rats treated with either L-Arginine (10mg/kg/day) or fed soy enriched diet (200 g/kg diet) for 12 weeks. L-Arginine and soy enriched diet normalized serum PTH level and increased serum osteocalcin level; bone osteocalcin, osteoprotegerin and runt-related transcription factor2 mRNA levels compared to diabetic rats. A decrease in serum pyridinoline, C-terminal telopeptides of type I collagen, cathepsin k levels and bone cathepsin k mRNA level was observed in both treated groups. Both treatments increased serum insulin and insulin like growth factor-1 levels and decreased urinary calcium excretion.
CONCLUSIONS:
In conclusion, L-Arginine and soy enriched diet are effective in prevention of osteoporosis associated with diabetes mellitus.