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. 2004 Feb;25(1):49–68.

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The contents of articles or advertisements in The Clinical Biochemist – Reviews are not to be construed as official statements, evaluations or endorsements by the AACB, its official bodies or its agents. Statements of opinion in AACB publications are those of the contributors. Print Post Approved - PP255003/01665. Copyright © 2005 The Australasian Association of Clinical Biochemists Inc. No literary matter in The Clinical Biochemist – Reviews is to be reproduced, stored in a retrieval system or transmitted in any form by electronic or mechanical means, photocopying or recording, without permission. Requests to do so should be addressed to the Editor. ISSN 0159 – 8090

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Cholesterol metabolism and pathways in the hepatocyte. The cholesterol pool receives cholesterol from the blood through the LDL receptor (LDLR), LRP and SRB1. Additional inputs to the cholesterol pool are from CE by NCEH and de novo synthesis from AcCoA involving HMG-CoA reductase. Outputs of cholesterol from the pool are to lipoproteins as free cholesterol (FC), and CE by the reaction of cholesterol with non-esterified fatty acid (NEFA) catalysed by ACAT2. ACAT1 catalyses esterification of cholesterol for intracellular storage and cytochrome P₄₅₀7A (CYP7A) initiates bile acid synthesis. Lipoprotein assembly in the lumen of the ER involves (PL) and TG, apoB and MTP. The lipoproteins synthesised by the liver include VLDL₁ and VLDL₂, IDL and LDL. The ligand for internalisation of IDL is apoE (E) and for internalisation of LDL is apoB100 (B).