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Gastroenterology
Volume 137, Issue 3
, Pages
775-778
, September 2009
Intestinal Lipid Absorption, GLP-2, and CD36: Still More Mysteries to Moving Fat
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GLP2 enhances intestinal lipid absorption, but how? GLP-2 (triangles) binds its receptor (GLP-2R) on intestinal L cells, generating mediators including IGF-1, which signals via IGF-1 receptors (IGF-1R
GLP2 enhances intestinal lipid absorption, but how? GLP-2 (triangles) binds its receptor (GLP-2R) on intestinal L cells, generating mediators including IGF-1, which signals via IGF-1 receptors (IGF-1R) on epithelial cells. These various signals promote CD36 glycosylation, in turn altering epithelial long chain FA (LCFA) and monoacylglycerol (MAG) processing into TG via diacylglycerol acyltransferase 1 (Dgat1) and monoacylglycerol acyltransferase (Mgat). The rate-limiting step in CM formation is fusion of nascent apolipoprotein B48 (apoB48) with the luminal endoplasmic reticulum (ER) chaperone Mttp. GLP-2–mediated enhancement of intestinal lipid transport was attenuated in Cd36–/– mice, but further work is required to define the mechanisms involved.
Conflicts of interest The authors disclose no conflicts.
Funding Grant awards HL-38180, DK-56260 and DK-52574 to NOD.
PII: S0016-5085(09)01190-1
doi: 10.1053/j.gastro.2009.07.034
© 2009 AGA Institute. Published by Elsevier Inc. All rights reserved.
« Previous
Next »
Gastroenterology
Volume 137, Issue 3
, Pages
775-778
, September 2009

