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Regulating intestinal function to reduce atherogenic lipoproteins.

M Mahmood Hussain1, Tung Ming Leung1, Liye Zhou1

  • 1Department of Cell Biology, SUNY Downstate Medical Center, Brooklyn, NY 11797, USA ; Department of Pediatrics, SUNY Downstate Medical Center, Brooklyn, NY 11797, USA.

Clinical Lipidology
|January 11, 2014
PubMed
Summary

Accumulation of dietary fat in the blood, specifically intestine-derived lipoproteins, may drive atherosclerosis. Reducing intestinal lipid absorption could be a strategy to lower this risk.

Keywords:
MTPapoBatherosclerosischolesterolchylomicronemiahyperlipidemiahypertriglyceridemialipoproteinstriglyceride

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Area of Science:

  • Cardiovascular Biology
  • Lipid Metabolism

Background:

  • Dietary fat absorption and transport involve complex molecular pathways.
  • Accumulation of intestine-derived lipoproteins in circulation is increasingly linked to atherosclerosis development.

Purpose of the Study:

  • To review current knowledge on dietary lipid metabolism.
  • To examine evidence from mouse models supporting the role of intestinal lipoproteins in atherosclerosis.

Main Methods:

  • Analysis of studies involving genetic modifications in mice affecting lipoprotein metabolism and atherosclerosis.
  • Review of molecular mechanisms underlying intestinal lipoprotein interaction with the vasculature.

Main Results:

  • Defects in lipoprotein catabolism (e.g., lipoprotein lipase, Gpihbp1 deficiencies) increase atherosclerosis.
  • Overproduction of intestinal lipoproteins (e.g., in inositol-requiring enzyme 1β-deficient mice) exacerbates atherosclerosis.
  • Intestinal lipoproteins promote inflammation and macrophage activation, contributing to atherosclerotic plaque.

Conclusions:

  • Both overproduction and reduced catabolism of intestinal lipoproteins contribute to atherosclerosis.
  • Targeting intestinal lipid absorption presents a potential therapeutic approach for reducing atherosclerosis.