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Increased intestinal lipid absorption caused by Ire1? deficiency contributes to hyperlipidemia and atherosclerosis in apolipoprotein E-deficient mice.


ABSTRACT: 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.This study aims to delineate whether changes in intestinal lipid absorption associated with loss of inositol-requiring enzyme 1? (Ire1?) would affect the development of hyperlipidemia and atherosclerosis in Apoe(-/-) mice.We used Ire1?-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.These studies indicate that Ire1? regulates intestinal lipid absorption and that increased intestinal lipoprotein production contributes to atherosclerosis.

SUBMITTER: Iqbal J 

PROVIDER: S-EPMC3384494 | biostudies-literature | 2012 Jun

REPOSITORIES: biostudies-literature

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Increased intestinal lipid absorption caused by Ire1β deficiency contributes to hyperlipidemia and atherosclerosis in apolipoprotein E-deficient mice.

Iqbal Jahangir J   Queiroz Joyce J   Li Yan Y   Jiang Xian-Cheng XC   Ron David D   Hussain M Mahmood MM  

Circulation research 20120503 12


<h4>Rationale</h4>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.<h4>Objective</h4>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.<h4>Methods and results</h4>We used Ire  ...[more]

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