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(Circulation Research. 2008;102:e119.)
© 2008 American Heart Association, Inc.

Letters to the Editor

Response to the Letter by Ebara et al

George Liu

Institute of Cardiovascular Sciences, Peking University, Beijing, China

Michael R. Hayden

Department of Medical Genetics, University of British Columbia, Centre for Molecular Medicine and Therapeutics, Vancouver, Canada, E-mail mrh@cmmt.ubc.ca

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

As highlighted by Dr Ebara et al, there are key differences in lipoprotein metabolism between mice and humans. In humans, lipoprotein lipase (LPL) deficiency with severe hypertriglyceridemia was originally reported to be nonatherogenic.¹ However, in 1996, Benlian et al presented 4 French cases of LPL deficiency with severe hypertriglyceridemia who all displayed various degrees of angiographically defined coronary or carotid atherosclerosis.² One of them had bypass surgery at age 65, and during the surgery, atherosclerotic lesions of all grades (from fatty streaks to calcified and hemorrhagic atherosclerotic plaques) were noted all along the aorta and iliac and femoral arteries. The patient died suddenly 2 years after surgery. These 4 cases not only exhibited severe hypertriglyceridemia, but they also had high cholesterol levels, which were elevated 3- to 4-fold over the normal range, because even in triglyceride-rich lipoproteins, there is a certain portion of cholesterol and its esters consisting of lipid core.

Over the past decade, there have been several case reports of LPL-deficient patients with or without detectable lesions of atherosclerosis.^3,4 Therefore, humans with LPL-deficient hypertriglyceridemia appear to be prone to atherosclerosis in certain circumstances. As discussed in our article,⁵ such discrepancies between different individuals may be partially explained by the presence or absence of noncatalytic LPL protein. The catalytically inactive LPL protein could act as a molecular bridge between proteoglycans and different lipoprotein receptors to facilitate lipoprotein uptake by cells such as macrophages. Therefore, if macrophage secrete inactive LPL protein, such molecules may then enhance foam cell formation through . . . [Full Text of this Article]