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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:1538.)
© 2004 American Heart Association, Inc.

Editorials

Unique Pathway for Cholesterol Uptake in Fat Cells

Sergio Fazio; MacRae F. Linton

From the Division of Cardiovascular Medicine, Department of Medicine (S.F., M.F.L.), and the Departments of Pathology (S.F.) and Pharmacology (M.F.L.), Vanderbilt University Medical Center, Nashville, Tenn.

Correspondence to Sergio Fazio, MD, PhD, or MacRae F. Linton, MD, Vanderbilt University Medical Center, Division of Cardiovascular Medicine, 383 PRB, Nashville, TN 37232-6300.E-mail sergio.fazio@vanderbilt.edu or macrae.linton@vanderbilt.edu

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

The biologic features of high-density lipoprotein (HDL) cholesterol delivery to the cell have mostly been investigated in hepatocytes, the consensus termination point of the reverse cholesterol transport pathway. It has long been known that the delivery of HDL cholesterol to the hepatocyte does not involve the internalization and degradation of the lipoprotein particle, as is the case for the apolipoprotein (apo)B-containing lipoproteins, but rather it is based on the selective unloading of the cholesterol cargo from the particle into the cell.¹ With the discovery that the scavenger receptor type BI (SR-BI) acts as the hepatic HDL receptor,² the final events of HDL cholesterol delivery have been well characterized: HDL binds to SR-BI through apolipoprotein AI (apoAI), the cholesteryl ester (CE) cargo of HDL is selectively unloaded into the cell where it is trafficked back into forming lipoproteins or into the bile, and the lipid-poor apoAI returns in the circulation for another round of peripheral cholesterol collection.³ Even though this appears to be a systemic mechanism for redistribution of peripheral cholesterol to a central organ in charge of cholesterol disposal, it is possible that alternative processes might have developed so that particular non-hepatic cell types can acquire needed cholesterol from the HDL.

See page 1669

Adipocytes might be unique in their need of acquiring cholesterol, because of their limited ability to synthesize their own.⁴ This can be caused by a preferential utilization of acetate for fatty acid synthesis or reduced efficiency of enzymes downstream of squalene synthase in the pathway of . . . [Full Text of this Article]

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