Abstract
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, develop hyperlipidemia, and have higher levels of atherosclerotic plaques compared to Apoe -/- mice when fed chow and western diets. In contrast, plasma cytokines were similar in Ire1b -/- /Apoe -/- and Apoe -/- mice. Conclusions: These studies indicate that Ire1β regulates intestinal lipid absorption and that increased intestinal lipoprotein production contributes to atherosclerosis.
Published Version
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