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Updated: May 22, 2026

Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
Increased intestinal lipid absorption caused by Ire1β deficiency contributes to hyperlipidemia and atherosclerosis in
Jahangir Iqbal1, Joyce Queiroz, Yan Li
1Department of Cell Biology, Box 5, SUNY Downstate Medical Center, 450 Clarkson Ave, Brooklyn, NY 11203, USA. jahangir.iqbal@downstate.edu
Rationale:
High fasting serum lipid levels are significant risk factors for atherosclerosis. However, the contributions of postprandial excursions in serum lipoproteins to atherogenesis are less well-characterized.
Objective:
This study aims to delineate whether changes in intestinal lipid absorption associated with loss of inositol-requiring enzyme 1β (Ire1β) would affect the development of hyperlipidemia and atherosclerosis in Apoe(-/-) mice.
Methods And Results:
We used Ire1β-deficient mice to assess the contribution of intestinal lipid absorption to atherosclerosis. Here, we show that Ire1b(-/-)/Apoe(-/-) mice contain higher levels of intestinal microsomal triglyceride transfer protein, absorb more lipids, exhibit hyperlipidemia, and have higher levels of atherosclerotic plaques compared with Apoe(-/-) mice when fed chow and western diets.
Conclusions:
These studies indicate that Ire1β regulates intestinal lipid absorption and that increased intestinal lipoprotein production contributes to atherosclerosis.
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