Cardiorespiratory/Metabolic Laboratory, The University of Memphis, Memphis, Tennessee 38152, USA.
Nutr Metab (Lond). 2009 Jun 2;6:25. doi: 10.1186/1743-7075-6-25.
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.
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.
ALCA, but not placebo, resulted in an increase in nitrate/nitrite (25.4 ± 1.9 to 30.1 ± 2.8 mumol·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 mumol.L⁻¹·6 hr⁻¹) to post (172.40 ± 21.75 mumol·L⁻¹·6 hr⁻¹) intervention with ALCA, and the magnitude of decrease following feeding was not as pronounced as with placebo.
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.
代谢紊乱(如糖尿病)患者的静息和餐后氧化应激升高。抗氧化剂补充剂可能会减轻进食后氧化应激的升高。因此,我们旨在确定精氨酸乙酰左旋肉碱(ALCA)对葡萄糖和脂质代谢以及氧化应激的静息和餐后生物标志物的影响。
29 名糖尿病前期的男性和女性被随机分配到 ALCA 组(n = 14;31 ± 3 岁)或安慰剂组(n = 15;35 ± 3 岁),以双盲设计,每天摄入 3 g·天⁻¹,持续八周。在干预前后,受试者均采集空腹血样。在每次空腹采样后,受试者均摄入高脂肪、高碳水化合物餐,并在餐后 1、2、4 和 6 小时再次采血。对各种代谢变量(如葡萄糖、HbA1c、血脂谱、C 反应蛋白、硝酸盐/亚硝酸盐和几种氧化应激标志物)进行分析。计算餐后测量的每个变量的曲线下面积(AUC),包括干预前后。
与安慰剂相比,ALCA 可使硝酸盐/亚硝酸盐(25.4 ± 1.9 至 30.1 ± 2.8 mumol·L⁻¹)在干预前后增加(p = 0.01),而干预后的数值高于安慰剂。没有其他有统计学意义的变化(p > 0.05),尽管 ALCA 使葡萄糖(109 ± 5 至 103 ± 5 mg·dL⁻¹)、HbA1c(6.6 ± 1.1 至 6.2 ± 1.2%)和 HOMA-IR(3.3 ± 1.3 至 2.9 ± 1.2)略有改善。ALCA 和安慰剂在任何变量的餐后 AUC 数据均无统计学差异(p > 0.05)。然而,硝酸盐/亚硝酸盐的变化具有中等的效应大小(r = 0.35),从干预前(139.50 ± 18.35 mumol·L⁻¹·6 hr⁻¹)到干预后(172.40 ± 21.75 mumol·L⁻¹·6 hr⁻¹)增加,并且与安慰剂相比,喂养后降低的幅度并不那么明显。
在糖尿病前期患者中,补充精氨酸乙酰左旋肉碱可导致静息状态下硝酸盐/亚硝酸盐增加,而静息或餐后测量的其他代谢或氧化应激变量无统计学意义的变化。