Research

Effect of oral acetyl L-carnitine arginate on resting and postprandial blood biomarkers in pre-diabetics

Richard J Bloomer , Kelsey H Fisher-Wellman and Patrick S Tucker

Cardiorespiratory/Metabolic Laboratory, The University of Memphis, Memphis, Tennessee 38152, USA

author email corresponding author email

Nutrition & Metabolism 2009, 6:25doi:10.1186/1743-7075-6-25

Published:	2 June 2009

Abstract

Background

Resting and postprandial oxidative stress is elevated in those with metabolic disorders such as diabetes. Antioxidant supplementation may attenuate the rise in oxidative stress following feeding. Therefore we sought to determine the effects of acetyl L-carnitine arginate (ALCA) on resting and postprandial biomarkers of glucose and lipid metabolism, as well as oxidative stress.

Methods

Twenty-nine pre-diabetic men and women were randomly assigned to either 3 g·day^-1 of ALCA (n = 14; 31 ± 3 yrs) or placebo (n = 15; 35 ± 3 yrs) in a double-blind design, to consume for eight weeks. Fasting blood samples were taken from subjects both pre and post intervention. After each fasting sample was obtained, subjects consumed a high fat, high carbohydrate meal and additional blood samples were taken at 1, 2, 4, and 6 hours post meal. Samples were analyzed for a variety of metabolic variables (e.g., glucose, HbA1c, lipid panel, C-reactive protein, nitrate/nitrite, and several markers of oxidative stress). Area under the curve (AUC) was calculated for each variable measured post meal, both pre and post intervention.

Results

ALCA, but not placebo, resulted in an increase in nitrate/nitrite (25.4 ± 1.9 to 30.1 ± 2.8 μmol·L^-1) from pre to post intervention, with post intervention values greater compared to placebo (p = 0.01). No other changes of statistical significance were noted (p > 0.05), although ALCA resulted in slight improvements in glucose (109 ± 5 to 103 ± 5 mg·dL^-1), HbA1c (6.6 ± 1.1 to 6.2 ± 1.2%), and HOMA-IR (3.3 ± 1.3 to 2.9 ± 1.2). AUC postprandial data were not statistically different between ALCA and placebo for any variable (p > 0.05). However, nitrate/nitrite demonstrated a moderate effect size (r = 0.35) for increase from pre (139.50 ± 18.35 μmol·L^-1·6 hr^-1) to post (172.40 ± 21.75 μmol·L^-1·6 hr^-1) intervention with ALCA, and the magnitude of decrease following feeding was not as pronounced as with placebo.

Conclusion

Supplementation with ALCA results in an increase in resting nitrate/nitrite in pre-diabetics, without any statistically significant change in other metabolic or oxidative stress variables measured at rest or post meal.