Lipid metabolism: Edited by Jeffrey S. CohnIntestinal lipoprotein overproduction in insulin-resistant statesAdeli, Khosrowa; Lewis, Gary FbAuthor Information aMolecular Structure and Function, Research Institute, The Hospital for Sick Children, Canada bDepartments of Medicine and Physiology, University of Toronto, Toronto, Ontario, Canada Correspondence to Khosrow Adeli, Molecular Structure and Function, Research Institute, The Hospital for Sick Children, University of Toronto, 555 University Avenue, Toronto, Ontario, M5G 1X8, Canada Tel: +1 416 813 8682; fax: +1 416 813 6257; e-mail: firstname.lastname@example.org Current Opinion in Lipidology: June 2008 - Volume 19 - Issue 3 - p 221-228 doi: 10.1097/MOL.0b013e3282ffaf82 Buy Metrics Abstract Purpose of review Excessive postprandial lipemia is highly prevalent in obese and insulin-resistant/type 2 diabetic individuals and substantially increases the risk of atherosclerosis and cardiovascular disease. This article will review our current understanding of the link between insulin resistance and intestinal lipoprotein overproduction and highlight some of the key recent findings in the field. Recent findings Emerging evidence from several animal models of insulin resistance as well as insulin-resistant humans clearly supports the link between insulin resistance and aberrant intestinal lipoprotein metabolism. In insulin-resistant states, elevated free fatty acid flux into the intestine, downregulation of intestinal insulin signaling and upregulation of microsomal triglyceride transfer protein all appear to stimulate intestinal lipoprotein production. Gut peptides, GLP-1 and GLP-2, may be important regulators of intestinal lipid absorption and lipoprotein production. Summary Available evidence in humans and animal models strongly favors the concept that the small intestine is not merely an absorptive organ but rather plays an active role in regulating the rate of production of triglyceride-rich lipoproteins. Metabolic signals in insulin resistance and type 2 diabetes and in some cases an aberrant intestinal response to these factors all contribute to the enhanced formation and secretion of triglyceride-rich lipoproteins. © 2008 Lippincott Williams & Wilkins, Inc.