Institutional members access full text with Ovid®

Share this article on:

Intestinal lipid absorption and lipoprotein formation

Hussain, M. Mahmooda,b,c

Current Opinion in Lipidology: June 2014 - Volume 25 - Issue 3 - p 200–206
doi: 10.1097/MOL.0000000000000084
LIPID METABOLISM: Edited by Ernst J. Schaefer

Purpose of review To summarize the evidence for the presence of two lipid absorption pathways and their regulation.

Recent findings Lipid absorption involves hydrolysis of dietary fat in the lumen of the intestine, followed by the uptake of hydrolyzed products by enterocytes. Lipids are resynthesized in the endoplasmic reticulum and are either secreted with chylomicrons and HDLs or stored as cytoplasmic lipid droplets. Lipids in the droplets are hydrolyzed and are secreted at a later time. Secretion of lipids by the chylomicron and HDL pathways are dependent on microsomal triglyceride transfer protein (MTP) and ATP-binding cassette family A protein 1, respectively, and are regulated independently. Gene-ablation studies showed that MTP function and chylomicron assembly is essential for the absorption of triglycerides. Ablation of MTP abolishes triglyceride absorption and results in massive triglyceride accumulation in enterocytes. Although the majority of phospholipid, cholesterol, and vitamin E are absorbed through the chylomicron pathway, a significant amount of these lipids are also absorbed via the HDL pathway. Chylomicron assembly and secretion is increased by the enhanced availability of fatty acids, whereas the HDL pathway is upregulated by liver X receptor agonists.

Summary Triglycerides are exclusively transported with chylomicrons and this process is critically dependent on MTP. In addition to chylomicrons, absorption of phospholipids, free cholesterol, retinol, and vitamin E also involves HDLs. These two pathways are complementary and are regulated independently. They may be targeted to lower lipid absorption in order to control hyperlipidemia, obesity, metabolic syndrome, steatosis, insulin resistance, atherosclerosis, and other disorders.

aDepartment of Cell Biology

bDepartment of Pediatrics, SUNY Downstate Medical Center

cVA New York Harbor Healthcare System, Brooklyn, New York, USA

Correspondence to M. Mahmood Hussain, Department of Cell Biology, SUNY Downstate Medical Center, 450 Clarkson Avenue, Brooklyn, NY 11203, USA. Tel: +1 718 270 4790; fax: +1 718 270 2462; e-mail:

© 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins