February 1, 1999Journal of Lipid ResearchOpen Access

In LDL receptor-deficient mice, catabolism of remnant lipoproteins requires a high level of apoE but is inhibited by excess apoE

View Full Paper

Ask AI

Bookmark

Population

Mice deficient for both endogenous Apoe and Ldlr genes (Apoe -/-. Ldlr -/-) and Apoe -/- mice

Comparison

Human APOE overexpression at various levels in… vs Different levels of APOE expression and Apoe -/…

Design

Preclinical

Authors

KDKo Willems van DijkLeiden University Medical Center BVBart J.M. van VlijmenLeiden University Medical Center HHH. Belinda van't HofJohannes Gutenberg University Mainz

Discussion

Member takes

Implication

May limit high-dose APOE therapies in severe hypercholesterolemia; extends apoE biology but needs human trials.

Structured PICO

Population

Mice deficient for both endogenous Apoe and Ldlr genes (Apoe -/-. Ldlr -/-) and Apoe -/- mice

Intervention

Human APOE overexpression at various levels (low, moderately high, very high) in the liver using adenovirus-mediated gene transfer

Comparator

Different levels of APOE expression and Apoe -/- mice

Outcome

Serum cholesterol and triglyceride levels, and VLDL clearancesurrogate

In LDL receptor-deficient mice, moderate apoE overexpression reduces cholesterol, but excessive apoE paradoxically causes severe hypertriglyceridemia by increasing VLDL production and inhibiting lipolysis.

Cite This Study

Dijk et al. (1999) studied this question.

synapsesocial.com/papers/6a7d1771c7e6f6a50737cd87 https://doi.org/10.1016/s0022-2275(20)33374-5

View Full Paper

Ask AI

Bookmark

In LDL receptor-deficient mice, catabolism of remnant lipoproteins requires a high level of apoE but is inhibited by excess apoE

Discussion

Member takes

Implication

Structured PICO

Cite This Study

In LDL receptor-deficient mice, catabolism of remnant lipoproteins requires a high level of apoE but is inhibited by excess apoE

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider