What question did this study set out to answer?

To determine whether the very low density lipoprotein receptor is necessary for optimal lipoprotein lipase actions in vivo and whether its deficiency worsens hypertriglyceridemia.

March 1, 2002Journal of Biological ChemistryOpen Access

Very Low Density Lipoprotein (VLDL) Receptor-deficient Mice Have Reduced Lipoprotein Lipase Activity

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Population

VLDL receptor knockout mice, heterozygous LpL-deficient mice, and human apolipoprotein B transgenic mice

Comparison

VLDLr deficiency and infection with… vs Wild type/control mice

Design

Preclinical

Authors

HYHiroaki YagyuNational Hospital Organization Mito Medical Center ELErlo LutzUniversidade do Oeste de Santa Catarina YKYuko KakoChiba Hospital

Discussion

Member takes

Implication

VLDLr disruption impairs triglyceride clearance in mice; hypothesis-generating for its role in human LpL regulation and hypertriglyceridemia.

Key Points

To determine whether the very low density lipoprotein receptor is necessary for optimal lipoprotein lipase actions in vivo and whether its deficiency worsens hypertriglyceridemia.
Evaluated plasma triglyceride levels and lipoprotein profiles in fasted VLDL receptor-knockout (VLDLr0) mice crossed with heterozygous lipoprotein lipase-deficient (LpL1) and human apolipoprotein B transgenic mice.
Conducted [3H]VLDL turnover clearance assays and measured lipoprotein lipase activity in postheparin plasma, skeletal muscle, and cardiac tissue.
Injected wild-type and VLDLr0 mice with an adenovirus expressing receptor-associated protein to assess specific receptor inhibition.
Fasted VLDLr0 mice exhibited a 2-fold increase in triglyceride levels compared to controls, with hypertriglyceridemia further aggravated in LpL1 and apolipoprotein B transgenic backgrounds due to elevated apoB48-VLDL.
VLDLr0/LpL1 mice demonstrated a 50% reduction in VLDL-triglyceride clearance compared to LpL1 controls, alongside significantly reduced lipoprotein lipase activity in postheparin plasma, heart, and muscle tissue.
Adenovirus-mediated expression of receptor-associated protein reduced lipoprotein lipase activity in wild-type mice, but caused no further reduction in VLDLr0 mice.

Structured PICO

Population

VLDL receptor (VLDLr) knockout mice (VLDLr0), heterozygous LpL-deficient (LpL1) mice, and human apolipoprotein B (apoB) transgenic mice

Intervention

VLDLr deficiency (knockout) and infection with adenovirus-expressing receptor-associated protein (an inhibitor of the VLDLr)

Comparator

Wild type/control mice

Outcome

Triglyceride levels, VLDL-triglyceride clearance, and lipoprotein lipase (LpL) activitysurrogate

The VLDL receptor is required for normal lipoprotein lipase regulation in vivo, and its disruption leads to hypertriglyceridemia associated with decreased LpL activity.

Cite This Study

Yagyu et al. (2002) studied this question.

synapsesocial.com/papers/6a71877cac440176ef2a3155 https://doi.org/10.1074/jbc.m109966200

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Implication

VLDLr disruption impairs triglyceride clearance in mice; hypothesis-generating for its role in human LpL regulation and hypertriglyceridemia.

Very Low Density Lipoprotein (VLDL) Receptor-deficient Mice Have Reduced Lipoprotein Lipase Activity

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Very Low Density Lipoprotein (VLDL) Receptor-deficient Mice Have Reduced Lipoprotein Lipase Activity

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

Also Consider