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J. Lipid Res., doi:10.1194/jlr.M500212-JLR200
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Submitted on May 25, 2005
Revised on July 20, 2005
Accepted on August 2, 2005

Decreased adiponectin levels in familial combined hyperlipidemia patients contribute to the atherogenic lipid profile

Gerly M. van der Vleuten, Lambertus J. H. van Tits, Martin den Heijer, Heidi Lemmers, Anton F. H. Stalenhoef, and Jacqueline de Graaf

Department of General Internal Medicine 541, Radboud University Nijmegen Medical Centre, Nijmegen 6500 HB

Corresponding Author: G.vandervleuten{at}aig.umcn.nl

Objectives Familial combined hyperlipidemia (FCH) is characterized by elevated levels of total cholesterol, triglycerides and/or apolipoprotein B. Other features of FCH are obesity and insulin resistance. Adiponectin is a secretory product of the adipose tissue. Low levels of adiponectin are associated with insulin resistance and accelerated atherosclerosis. The aim of this study was to determine whether decreased adiponectin levels are associated with FCH and its phenotypes. Methods and Results The study population comprised 644 subjects, including 158 patients with FCH. Serum adiponectin levels were determined using a commercially available ELISA. For both males and females, the mean adiponectin level (µg/ml) was significantly lower in FCH patients (2.0 (1.8-2.2) and 2.5 (2.3-2.8), respectively) compared to normolipidemic relatives (2.3 (2.2-2.5) and 3.1 (2.8-3.3), respectively), and spouses (2.4 (2.1-2.7) and 3.2 (2.8-3.6), respectively), even after adjusting for waist circumference and insulin resistance. Low adiponectin level in FCH patients was a superior independent predictor of the atherogenic lipid profile, including high triglyceride levels, low HDL-cholesterol levels and the amount of small dense LDL present, compared to both obesity and insulin resistance. Conclusions Low adiponectin levels may contribute to the atherogenic lipid profile in FCH, independent of insulin resistance and of obesity, as measured by waist circumference. This finding implies a role of adipose tissue metabolism in the pathophysiology of FCH.


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