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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:e143.)
© 2004 American Heart Association, Inc.

Letters to the Editor

Common Polymorphism in the MTP Promoter Attenuates the Dyslipidemic and Proatherogenic Effects of Excess Body Weight

Andrei C. Sposito; Sophie Gonbert; Gerard Turpin; M. John Chapman; Joëlle Thillet

Dyslipoproteinemia and Atherosclerosis Research Unit (A.C.S., S.G., M.J.C., J.T.), National Institute for Health and Medical Research (INSERM), Paris, France;, Heart Institute (InCor), Zerbini Foundation (A.C.S.), Brasilia, Brazil;, Department of Endocrinology and Metabolism (S.G., G.T.), APHP Hôpital de La Pitié-Salpetrière, France

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

In overweight subjects, an elevated supply of intracellular lipid stimulates the microsomal triglyceride transfer protein (MTP)-dependent assembly of apoB-containing lipoproteins in both intestinal and hepatic tissues, with subsequent secretion into the circulation. The severity of the dyslipidemia which results is however highly variable among overweight subjects, suggesting that genetic background may modulate the dyslipidemic effect of excess weight. In this context, a functional polymorphism in the MTP gene promoter region was recently described in which homozygotes for a G-to-T substitution, located 493 bp upstream from the transcription initiation site, display lower plasma levels of apoB-containing lipoproteins than carriers of the –493G allele. Hypothetically, such a functional polymorphism of the MTP promoter may attenuate the dyslipidemic effects of excess body weight and, in this way, equally attenuate the development of atherosclerotic disease in overweight subjects. We evaluated this hypothesis in 326 normotensive nondiabetic subjects with a broad range of body mass indices (BMI; 16.6 to 40.0kg/m²) who were consecutively evaluated at the Endocrinology Department of La Pitié-Salpetriere Hospital in Paris, France and were considered to be at low cardiovascular risk (n=189) or were enrolled as healthy volunteers in the Stanislas Cohort, Nancy, France (n=137). The MTP –493G/T promoter genotype was determined as described by Karpe et al.¹ Plasma levels of total cholesterol and triglycerides were determined by nephelometry, and HDL-cholesterol concentration was determined enzymatically with a commercially available kit (Biomerieux). Ultrasonographic evaluation of the extracranial carotid arteries was performed with a duplex system (ACUSON Sequoia 512). The . . . [Full Text of this Article]