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Randomized Controlled Trial
. 2016 Oct 28;17(11):1802.
doi: 10.3390/ijms17111802.

A Clinical Trial about a Food Supplement Containing α-Lipoic Acid on Oxidative Stress Markers in Type 2 Diabetic Patients

Affiliations
Randomized Controlled Trial

A Clinical Trial about a Food Supplement Containing α-Lipoic Acid on Oxidative Stress Markers in Type 2 Diabetic Patients

Giuseppe Derosa et al. Int J Mol Sci. .

Abstract

The aim of this study was to evaluate the effect of a food supplement containing α-lipoic acid and of a placebo on glyco-metabolic control and on oxidative stress markers in type 2 diabetics. We randomized 105 diabetics to either a supplementation containing 600 mg of α-lipoic acid, 165 mg of L-carnosin, 7.5 mg of zinc, and vitamins of group B, or a placebo, for three months. We evaluated body mass index, fasting plasma glucose (FPG), post-prandial-glucose (PPG), glycated hemoglobin (HbA1c), fasting plasma insulin (FPI), HOMA-index (HOMA-IR), lipid profile, high sensitivity C-reactive protein (Hs-CRP), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA). There was a reduction of FPG, PPG, and HbA1c with the food supplement containing α-lipoic acid compared with a baseline, and with the placebo. Concerning lipid profile, we observed a reduction of LDL-C, and Tg with the food supplement, compared with both the baseline, and the placebo. There was a reduction of Hs-CRP with the food supplement containing α-lipoic acid, both compared with the baseline and the placebo. An increase of SOD, and GSH-Px, and a decrease of MDA were reached by the food supplement containing α-lipoic acid, both compared with the baseline and the placebo. We can conclude that the food supplement containing α-lipoic acid, L-carnosin, zinc, and vitamins of group B improved glycemic control, lipid profile, and anti-oxidative stress markers.

Keywords: L-carnosin; malondialdehyde; oxidative stress; α-lipoic acid.

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Conflict of interest statement

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties. No writing assistance was utilized in the production of this manuscript.

Figures

Figure 1
Figure 1
Biological functions of α-lipoic acid. α-lipoic acid (ALA) and its reduced form dihydrolipoic acid (DHLA) create a potent redox couple, often called a “universal anti-oxidant” for its capacity to regenerate several others anti-oxidants, such as vitamins C and E and glutathione. α-lipoic acid is also able to directly scavenge ROS, possesses metal chelating activity, and enhances the mitochondrial expression of key anti-oxidant enzymes. Through these properties, α-lipoic acid exerts different activities, from mitochondrial bioenergetics cofactor to stress response regulation and neuronal protection. Mitochondrial bioenergetic cofactor: α-lipoic acid is a key cofactor for mitochondrial bioenergetic enzymes, including pyruvate dehydrogenase and α-ketoglutarate dehydrogenase complexes, stimulating glucose and lipid metabolism. It acts as an insulin-mimetic agent, regulating the IR/PI3K/Akt pathway, so it enhances the uptake and the utilization of glucose, improving glycemic control. Stress response regulation: α-lipoic acid responds to stress factors, inhibiting stress induced transcription factor activation, such as NF-κB and AP-1, and modulating pro-inflammatory signaling, hence the anti-inflammatory activity. Neuronal protection: it is also well known that α-lipoic acid improves diabetic polyneuropathies, while attention has only recently been focused on the capacity to attenuate the hyperalgesia through the modulation of T-type calcium and transient receptor potential (TRPA1) channels.

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