Gastroenterology
Volume 137, Issue 3 , Pages 775-778 , September 2009

Intestinal Lipid Absorption, GLP-2, and CD36: Still More Mysteries to Moving Fat

  • Elizabeth P. Newberry
  • ,
  • Nicholas O. Davidson

      Affiliations

    • Corresponding Author InformationReprint requests Address requests for reprints to: Nicholas O. Davidson, MD, Division of Gastroenterology, Box 8124, Washington University School of Medicine, 660 Euclid Avenue, St. Louis, Missouri 63110. phone: (314) 362-2027

  • Image Result

    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

Gastroenterology
Volume 137, Issue 3 , Pages 775-778 , September 2009