October 1, 2000Journal of Biological ChemistryOpen Access

A Targeted Apolipoprotein B-38.9-producing Mutation Causes Fatty Livers in Mice Due to the Reduced Ability of Apolipoprotein B-38.9 to Transport Triglycerides

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Population

Engineered mice bearing a premature stop codon at residue 1767 and a 42-base pair loxP inserted into intron…

Design

Preclinical

Authors

ZCZhouji ChenDiscovery Institute RFRobin L. FitzgeraldWashington University in St. Louis MAMaurizio AvernaUniversity of Rome Tor Vergata

Discussion

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Implication

Offers murine model of hypobetalipoproteinemia; leaves open translation to human fatty-liver mechanisms.

Structured PICO

Population

Engineered mice bearing a premature stop codon at residue 1767 and a 42-base pair loxP inserted into intron 24 of the apo B gene (apob(38.9/38.9) homozygotes and apob(+/)(38.9) heterozygotes) and cultured hepatocytes.

Intervention

Targeted apo B-38.9-producing mutation

Outcome

Apo B protein and mRNA levels, synthesis and secretion rates, hepatic triglyceride secretion rates, and presence of fatty liverssurrogate

The apo B-38.9 mutation in mice causes fatty livers due to a reduced capacity of the truncated apolipoprotein for triglyceride transport, providing a faithful model for familial hypobetalipoproteinemia.

Cite This Study

Chen et al. (2000) studied this question.

synapsesocial.com/papers/6a769aa95c9af0cec87d20dc https://doi.org/10.1074/jbc.m004913200

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A Targeted Apolipoprotein B-38.9-producing Mutation Causes Fatty Livers in Mice Due to the Reduced Ability of Apolipoprotein B-38.9 to Transport Triglycerides

Discussion

Member takes

Implication

Structured PICO

Cite This Study

A Targeted Apolipoprotein B-38.9-producing Mutation Causes Fatty Livers in Mice Due to the Reduced Ability of Apolipoprotein B-38.9 to Transport Triglycerides

Discussion

Member takes

Implication

Structured PICO

Cite This Study

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