What are the key findings of this study?

In vitro lipolysis of VLDL from familial dysbetalipoproteinemic plasma resulted in 95% in normolipidemic VLDL, indicating resistance to lipoprotein lipase.

What question did this study set out to answer?

The study aims to investigate the resistance of very low density lipoprotein (VLDL) from familial dysbetalipoproteinemia to in vitro lipolytic conversion to low density lipoprotein (LDL).

September 1, 1983Journal of Lipid ResearchOpen Access

Resistance of a very low density lipoprotein subpopulation from familial dysbetalipoproteinemia to in vitro lipolytic conversion to the low density lipoprotein density fraction.

Q: What is the clinical evidence from this study?

Population: Familial dysbetalipoproteinemia. Intervention: In vitro lipolysis by purified bovine milk lipoprotein lipase vs. Normolipidemic VLDL. Primary outcome: Removal of VLDL cholesterol from the VLDL density region.

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Key result

In vitro lipolysis of VLDL from familial dysbetalipoproteinemic plasma resulted in <50% cholesterol removal compared to >95% in normolipidemic VLDL, indicating resistance to lipoprotein lipase.

Key Points

The study aims to investigate the resistance of very low density lipoprotein (VLDL) from familial dysbetalipoproteinemia to in vitro lipolytic conversion to low density lipoprotein (LDL).
In vitro lipolysis of VLDL using purified bovine milk lipoprotein lipase was performed.
A combination of single vertical spin and vertical autoprofile methods was utilized for lipoprotein analysis.
Comparison of lipolysis responses between normolipidemic and familial dysbetalipoproteinemic VLDL was analyzed.
Greater than 95% of VLDL cholesterol transformed to LDL/HDL in normolipidemic plasma; less than 50% conversion in dysbetalipoproteinemic VLDL.
Lipoprotein lipase-resistant VLDL from dysbetalipoproteinemic plasma had higher cholesteryl ester and specific apolipoproteins (apoB, apoE).
Normolipidemic VLDL competes better for lipoprotein lipase, leading to superior lipolysis efficiency compared to dysbetalipoproteinemic VLDL.

Structured PICO

Population

In vitro model using very low density lipoprotein (VLDL) from normolipidemic and familial dysbetalipoproteinemic plasma

Intervention

In vitro lipolysis by purified bovine milk lipoprotein lipase

Comparator

VLDL from normolipidemic plasma

Outcome

Transformation of VLDL to LDL and transfer of cholesterol and proteinsurrogate

Familial dysbetalipoproteinemic VLDL contains a subpopulation resistant to lipoprotein lipase conversion to LDL, contributing to elevated cholesteryl ester-rich VLDL and IDL in these patients.

Discussion

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Implication

May explain remnant accumulation in dysbetalipoproteinemia; leaves open LPL resistance as a therapeutic target.

Cite This Study

Chung et al. (1983) studied Familial dysbetalipoproteinemia. In vitro lipolysis by purified bovine milk lipoprotein lipase vs. Normolipidemic VLDL was evaluated on Removal of VLDL cholesterol from the VLDL density region. In vitro lipolysis of VLDL from familial dysbetalipoproteinemic plasma resulted in <50% cholesterol removal compared to >95% in normolipidemic VLDL, indicating resistance to lipoprotein lipase.

synapsesocial.com/papers/6a22a8ef65451dc9090e0d3d https://doi.org/10.1016/s0022-2275(20)37898-6

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Resistance of a very low density lipoprotein subpopulation from familial dysbetalipoproteinemia to in vitro lipolytic conversion to the low density lipoprotein density fraction.

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Resistance of a very low density lipoprotein subpopulation from familial dysbetalipoproteinemia to in vitro lipolytic conversion to the low density lipoprotein density fraction.

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Also Consider