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Metformin reduces vascular endothelial dysfunction caused by an acute glucose load in patients with hypertension

Zhang TX, Xu JX, Peng F, Chai DJ, Lin JX

Blood pressure, 2013

34 participants

Abstract

BACKGROUND: To investigate the effects of a single dose of metformin (MF) on endothelium-dependent vasodilatation and serum antioxidant and free fatty acid levels in patients with primary hypertension (PH) after an acute glucose load.

MATERIALS AND METHODS: Patients with untreated PH were randomized to a no-metformin group (PH, n = 34) and a metformin group (PH+ MF, n = 28) who received a single dose of 500 mg metformin before testing. Healthy volunteers (n = 31) served as a control group. Brachial artery endothelium-dependent flow-mediated vasodilatation (FMD) was determined at 0, 1, 2 and 3 h after glucose load. Levels of serum superoxide dismutase (SOD), total antioxidant capacity (T-AOC), anti-superoxide anion free radical (AntiO2) and free fatty acids (FFA) were measured.

RESULTS: The FMD in the PH group decreased significantly 1 h after glucose load (PH: 10.9 ± 2.9% vs 13.67 ± 3.42% before glucose load). Metformin inhibited the effects of glucose load on FMD. At 1 h after acute glucose load, the concentrations of SOD, T-AOC and AntiO2 in the PH group decreased significantly compared with their fasting levels, and metformin inhibited the acute glucose load-induced decline in SOD and T-AOC levels.

CONCLUSIONS: Metformin can prevent transient endothelial dysfunction caused by acute glucose load in patients with PH.

How strong is the evidence?

Evidence Hub reads this as a randomized trial, done in people. Its evidence level is 2 of 5 (High · randomized trial). Randomized trials of a reasonable size are the strongest single-study design. Reported size: 34 participants or records.

How the five levels of evidence work. The level is assigned automatically from the abstract and can be wrong, so check the paper.

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