Impact of thioctic acid on glycemic indices and associated inflammatory-induced endothelial dysfunction in patients
Marwa S Al-Nami1, Hayder M Al-Kuraishy1, Ali I Al-Gareeb1
1Department of Pharmacology, Toxicology and Medicine, College of Medicine, Almustansiriya University, Baghdad, Iraq.
Objective:
To evaluate the effects of thioctic acid (TA) add-on metformin therapy on glycemic indices and associated inflammatory reactions induced-endothelial dysfunction (ED) in patients with type 2 diabetes mellitus (T2DM).
Methods:
In this case-control clinical study, a total number of 70 patients with T2DM compared with 30 healthy controls were divided into three groups: Group A (n = 30), healthy controls; Group B (n = 36), T2DM patients on metformin and Group C (n = 34), T2DM patients on metformin plus TA 600 mg/day. Anthropometric measurements, lipid profile, and routine biochemical variables were estimated. Serum human vascular cell adhesion molecule-1 (VCAM-1) and E-selectin were measured before and after 10 consecutive week's therapy with metformin and/or TA.
Results:
Metformin therapy led to significant reduction of fasting insulin and insulin resistance (IR) with an increment in the insulin sensitivity (P < 0.01). Metformin therapy improved lipid profile compared to the baseline (P < 0.01) with significant reduction of atherogenic index. Metformin plus TA therapy reduced fasting blood glucose, glycated hemoglobin, and IR and showed increment in the insulin sensitivity (P < 0.01) with insignificant effect on fasting insulin (P = 0.09) compared with metformin monotherapy. sVCAM-1 level was high in patients with T2DM (3.74 ± 1.34 ng/ml) at baseline, which decreased by metformin monotherapy to 2.32 ± 0.67 ng/ml or metformin plus TA to 1.98 ± 0.31 ng/ml (P < 0.01), but metformin plus TA illustrated insignificant difference compared to metformin alone (P = 0.29).
Conclusion:
TA add on metformin therapy improves glycemic indices and associated inflammatory mediators in patients with T2DM through modulation of IR , IS , and direct direct anti-inflammatory effect.
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