Poster Topical Area: Dietary Bioactive Components

Location: Hall D

Poster Board Number: 312

P08-054 - Arginase Inhibition by Inositol-stabilized Arginine Silicate (ASI; Nitrosigine®); A Novel Mechanism by which ASI Enhances Arginine Bioavailability

Monday, Jun 11
8:00 AM – 3:00 PM

Objectives: Several studies have shown that inositol-stabilized arginine silicate (ASI; Nitrosigine®) clinically enhances blood levels of arginine and nitric oxide (NO), making it a popular ingredient in sports nutrition supplements. ASI increases plasma arginine by >70% compared to arginine hydrochloride (ArgHCl), and does so for a significantly longer duration (up to 6 hrs.), indicating that ASI is a more bioavailable form of arginine1. However, the mechanism by which ASI enhances plasma arginine levels more than ArgHCl is still unknown. This clinical trial was designed to explore the hypothesis that ASI enhances plasma arginine levels through the inhibition of arginase and asymmetric dimethylarginine (ADMA), as these enzymes are known to inhibit arginine levels and NO synthesis, respectively2,3.

Methods: To explore this hypothesis, human plasma samples were tested for arginase and ADMA levels after 15 days of supplementation with ASI or ArgHCl. Ten healthy males per treatment group, aged 18 to 40 years, with BMI ≥ 18.5 to < 25 kg/m2, were randomly assigned to take a single oral dose of ASI or ArgHCl (each containing a total of 500 mg of arginine) qd for 15 days. These subjects attended study visits on Days 1 and 15, with a 7-day washout period between test product administration. Fasting blood samples were collected pre-dose and at 0.5, 1, 1.5, 2, 3, 4, 5 and 6 hours post-dose for plasma arginine, arginase, and ADMA measurements.

Results: Study results show that after 15 days of supplementation, arginase levels were significantly different between the ASI and ArgHCl groups (p<0.05). At multiple time points after supplementation, arginase levels were reduced by ASI, whereas there were no changes detected after ArgHCl supplementation. ADMA levels did not differ between the ASI and ArgHCl groups, and did not change compared to baseline.

Conclusions: The results of this study show that ASI supplementation inhibits arginase levels, but not ADMA levels, whereas ArgHCl does not significantly affect either enzyme. These results support the findings that ASI supplementation, after single dose (1 day) and multiple doses (15 days), inhibits the metabolic pathway that catabolizes arginine, thereby enhancing arginine bioavailability, and in turn, increases NO expression.

Funding Source: This study was funded by Nutrition 21, LLC.

CoAuthors: Sara Perez Ojalvo – Nutrition 21, LLC; Sarah Sylla – Nutrition 21, LLC; Emir Veledar – Emory University

James Komorowski

Chief Science Officer
Nutrition 21, LLC
Purchase, New York