Journal
EUROPEAN JOURNAL OF INTEGRATIVE MEDICINE
Volume 17, Issue -, Pages 112-118Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.eujim.2017.12.008
Keywords
Metabolic syndrome; Artichoke leaf extract; Cholesterol ester transfer protein; Taq IB polymorphism; Lipid profile; Randomised controlled
Categories
Funding
- Research Vice Chancellor, Tabriz University of Medical Sciences, Tabriz, Iran [5/97/4653]
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Introduction: The potentially favorable effects of artichoke leaf extract (ALE) have been shown on lipid profile; however, results are inconsistent. Taq IB polymorphism in cholesteryl ester transfer protein (CETP) gene may modulate the response to intervention. This study was aimed to examine the effects of ALE supplementation on serum lipid profile and CETP levels regarding CETP Taq IB polymorphism in patients with metabolic syndrome (MetS). Methods: In this double-blind placebo-controlled clinical trial, 80 patients with MetS were randomized to receive ALE (1800 mg per day as four tablets) or matching placebo for 12 weeks. Serum levels of lipid profile and CETP, as well as physical activity levels were assessed before and after the intervention. Physical activity levels were measured using short form of the International Physical Activity Questionnaire (IPAQ-SF). Moreover, patients were genotyped for CETP Taq IB polymorphism. Results: Mean age and BMI of the patients was 38.91 +/- 6.90 years and 34.32 +/- 4.28 kg/m(2), respectively. Twenty-eight percent of the patients were male. ALE supplementation decreased serum triglyceride (TG) level compared to placebo over 12 weeks (-10% vs. -2%, p= 0.01). There was no interaction between CETP Taq IB genotype and response to ALE supplementation. The subgroup analysis showed that in men carriers of Taq IB-B1B1, LDL-C level significantly decreased in ALE group compared to the placebo group (-15% vs. 9%, p= 0.004). Conclusions: ALE supplementation decreased TG levels without intervention-genotype interaction in patients with MetS. However, men with Taq IB-B1B1 genotype indicated a reduction of LDL-C in response to ALE.
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