Endocrine Abstracts (2006) 11 P326

The effect of moxonodine on endothelial dysfunction in metabolic syndrome

Ayse Sertkaya Cikim1, Ergun Topal2, Kerim Cikim3, Ismail Temel4 & Ramaza Ozdemir2


1Inonu University Faculty of Medicine Department of Internal Medicine Division of Endocrinology and Metabolism, Malatya, Turkey; 2Inonu University Faculty of Medicine Department of Cardiology, Malatya, Turkey; 3Inonu University Faculty of Medicine Department of Internal Medicine, Malatya, Turkey; 4Inonu University Faculty of Medicine Department of Biochemistry, Malatya, Turkey; 5Inonu University Faculty of Medicine Department of Cardiology, Malatya, Tuvalu.


Introduction: Metabolic syndrome (MS) is a clustering of risk factors. Endothelial dysfunction has been reported in patients with MS and even in healthy obese individuals with a normal metabolic profile. Sympathetic activity commonly is increased in obese hypertensives, and moxonidine, is found to be effective in lowering blood pressure and improving insulin sensitivity. The aim of this study is to evaluate the efficacy of moxonidine on endothelial dysfunction in insulin-resistant obese patients.

Method: The study group was consisted of 52 patients, 26 (Group 1; 19 women, 7 men, mean age 40.6±5.0 yrs) were found to have mild hypertension and besides hypocaloric diet they were treated with moxonidine for three months. The remainders (Group 2; 16 women, 10 men, mean age 39.6±5.9 yrs) were followed up with calorie restriction solely. Anthropometric and metabolic features of the groups and flow mediated dilatation (FMD) were evaluated. Insulin resistance was calculated by homeostasis model assessment formula (HOMA) and quantative insulin sensitivity check index (QUICKI).

Results: Systolic and diastolic blood pressures (P=0.000) and waist circumference (P=0.29) were high, and QUICKI (P=0.04) and FMD (P=0.01 were) significantly low in Group 1. On the third month of the follow-up nearly all the study parameters were found to de improved within each group. Not only were the decrement in blood pressure, but improvement in metabolic and anthropometric chances with increment of FMD was significant in moxonidine treated group.

Conclusion: Despite most of the risk markers of MS was found to be improved with diet, moxonidine had an additive effect not only on body fat mass and insulin resistance but on improvement of FMD as well. Moxonidine can be proposed as a valuable molecule for treating mild/moderate hypertension in obese and insulin resistant patients with metabolic syndrome especially for the improvement of endothelial dysfunction.

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