Fenofibrate Therapy Ameliorates Fasting and Postprandial Lipoproteinemia, Oxidative Stress, and the Inflammatory Response in Subjects With Hypertriglyceridemia and the Metabolic Syndrome  

Oleh:

Rosenson, Robert S ; Wolff, David A. ; Huskin, Anna L ; Helenowski, Irene B. ; Rademaker, Alfred W.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Diabetes Care vol. 30 no. 08 (Aug. 2007), page 1945.
Topik: Clinical Care; Education; Nutrition; Psychosocial Research

Ketersediaan

Perpustakaan FK Nomor Panggil: D05.K.2007.03 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

OBJECTIVE—The aim of this study was to determine the effects of fenofibrate (160 mg/day) on fasting and postprandial lipoproteins, oxidized fatty acids, and inflammatory mediators in subjects with hypertriglyceridemia and the metabolic syndrome. RESEARCH DESIGN AND METHODS—Fifty-nine subjects with fasting hypertriglyceridemia (1.7 and <6.9 mmol/l) and two or more of the Adult Treatment Panel III criteria for the metabolic syndrome were randomly assigned to fenofibrate (160 mg/day) or placebo in a double-blind, controlled clinical trial. RESULTS—Fenofibrate treatment lowered fasting triglycerides (–46.1%, P < 0.0001) and postprandial (area under the curve) triglycerides (–45.4%, P < 0.0001) due to significant reductions in postprandial levels of large (–40.8%, P < 0.0001) and medium (–49.5%, P < 0.0001) VLDL particles. The number of fasting total LDL particles was reduced in fenofibrate-treated subjects (–19.0%, P = 0.0033) primarily due to reductions in small LDL particles (–40.3%, P < 0.0001); these treatment differences persisted postprandially. Fasting and postprandial oxidized fatty acids were reduced in fenofibrate-treated subjects compared with placebo-administered subjects (–15.3%, P = 0.0013, and 31.0%, P < 0.0001, respectively), and fenofibrate therapy lowered fasting and postprandial soluble vascular cell adhesion molecule-1 (VCAM-1) (–10.9%, P = 0.0005, and –12.0%, P = 0.0001, respectively) as well as fasting and postprandial soluble intercellular adhesion molecule-1 (ICAM-1) (–14.8%, P < 0.0001, and –15.3%, P < 0.0001, respectively). Reductions in VCAM-1 and ICAM-1 were correlated with reductions in fasting and postprandial large VLDL particles (P < 0.0001) as well as postprandial oxidized fatty acids (P < 0.0005). CONCLUSIONS—Triglyceride-lowering therapy with fenofibrate reduced fasting and postprandial free fatty acid oxidation and inflammatory responses, and these antiatherosclerotic effects were most highly correlated with reductions in large VLDL particles.

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