July 28, 2007Diabetes Care119 citations
View Full PaperFenofibrate Therapy Ameliorates Fasting and Postprandial Lipoproteinemia, Oxidative Stress, and the Inflammatory Response in Subjects With Hypertriglyceridemia and the Metabolic Syndrome
Key Result
Fenofibrate therapy significantly reduced fasting triglycerides (-46.1%, P<0.0001) and postprandial triglycerides (-45.4%, P<0.0001) in subjects with hypertriglyceridemia and metabolic syndrome.
Study Design
Type
RCT (n=59)
Blinding
Double-blind
Randomization
randomly assigned
Structured PICO
Does fenofibrate 160 mg/day improve fasting and postprandial lipoproteinemia, oxidative stress, and inflammatory markers in subjects with hypertriglyceridemia and metabolic syndrome?
P
Population
59 subjects with fasting hypertriglyceridemia and metabolic syndrome.
I
Intervention
Fenofibrate 160 mg/day
C
Comparator
Placebo
O
Outcome
Fasting and postprandial lipoproteins, oxidized fatty acids, and inflammatory mediatorssurrogate
Fenofibrate significantly reduces fasting and postprandial triglycerides, oxidized fatty acids, and inflammatory markers in patients with hypertriglyceridemia and metabolic syndrome.
Main Result
Effect estimate: -46.1% reduction
p-value: p=< 0.0001
Abstract
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 (> or = 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.