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Acetyl-L-Carnitine (ALC)

Reduces oxidative stress helps reduce metabolic disorders such as diabetes.

1. Wickipedia "Carnitine is a quaternary ammonium compound biosynthesized from the amino acids lysine and methionine.[1] In living cells, it is required for the transport of fatty acids from the cytosol into the mitochondria during the breakdown of lipids (or fats) for the generation of metabolic energy. It is often sold as a nutritional supplement. Carnitine was originally found as a growth factor for mealworms and labeled vitamin Bt. Carnitine exists in two stereoisomers: its biologically active form is L-carnitine, while its enantiomer, D-carnitine, is biologically inactive.[2]"

2. "Effect of oral acetyl L-carnitine arginate on resting and postprandial blood biomarkers in pre-diabetics.
Bloomer RJ, Fisher-Wellman KH, Tucker PS. Cardiorespiratory/Metabolic Laboratory, The University of Memphis, Memphis, Tennessee 38152, USA.

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 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 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. 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. " PMID: 19490608 PMID: 19490608

3. "Effect of short term treatment of L-carnitine on tissue ACE activity in streptozotocin-induced diabetic rats.
Sharifi AM, Zare B, Keshavarz M, Ghaderpanahi M. Department of Pharmacology and Cellular and Molecular Research Center, School of Medicine, Iran University of Medical Sciences, P.O. Box 14155-6183, Tehran, Iran; Endocrine and Metabolism Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran.

Diabetes is commonly related to the both microvascular as well as macrovascular complications. It appears that both metabolic and hemodynamic factors interact to create these problems. In this study the effects of orally administered L-carnitine, a natural amino acid, on ACE activity in streptozotocin (STZ)-induced diabetic rats were investigated. Streptozotocin (60mg/kg body weight) was given intraperitoneally. Fifty male Sprague-Dawley rats were divided into four groups: untreated normal (C), L-carnitine treated normal (CT), untreated diabetics (D), L-carnitine-treated diabetics (DT). CT and DT received daily L-carnitine 1g/kg orally for 3 weeks after inducing diabetes. The ACE activities in aorta, heart and kidney homogenates was measured at the end of 3 weeks. They were significantly increased in D compared to C group (P<0.05) and significantly decreased in aorta, heart and kidney in DT compared to D group. In conclusion, L-carnitine can reduce tissue ACE activity in aorta, heart and kidney in streptozotocin diabetic rats, which may be due to higher NO production." PMID: 19406626 PMID: 19406626




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