What question did this study set out to answer?

To assess in vivo whether dietary stress from an oral fat load unmasks catalytic defects in normolipidemic carriers of the lipoprotein lipase Asn291Ser mutation.

January 1, 1996Journal of Lipid ResearchOpen Access

A frequently occurring mutation in the lipoprotein lipase gene (Asn291Ser) results in altered postprandial chylomicron triglyceride and retinyl palmitate response in normolipidemic carriers.

View Full Paper

Ask AI

Bookmark

Why the study?

Does an oral fat load unmask catalytic defects in normolipidemic carriers of the Asn291Ser mutation in the LPL gene compared to healthy controls?

Population

9 subjects: 3 unrelated normolipidemic Asn291Ser carriers, 5 healthy controls, and 1 subject with a 50%…

Comparison

Oral fat load vs Healthy controls and a subject with a 50%…

Design

Case-control

Authors

SPSimon N. PimstoneUniversity of British Columbia SCSusanne M. CleeUniversity of British Columbia SGSéverine GagnéInstitut Agro Rennes-Angers

Discussion

Member takes

Implication

Postprandial testing may detect functional LPL impairment in normolipidemic carriers; hypothesis-generating and requires prospective validation before clinical consideration.

Key Points

To assess in vivo whether dietary stress from an oral fat load unmasks catalytic defects in normolipidemic carriers of the lipoprotein lipase Asn291Ser mutation.
Conducted an oral fat load challenge in 3 unrelated normolipidemic Asn291Ser mutation carriers, 5 healthy controls, and 1 subject with a 50% baseline reduction in lipoprotein lipase activity.
Measured postprandial chylomicron triglyceride and chylomicron retinyl palmitate peak concentrations and calculated areas under the response curve.
Asn291Ser carriers showed significantly higher postprandial peak concentrations of chylomicron triglycerides (P = 0.03) and chylomicron retinyl palmitate (P = 0.02) compared to healthy controls.
Total area under the response curve was significantly elevated in carriers for both chylomicron triglycerides (P = 0.02) and chylomicron retinyl palmitate (P = 0.01) relative to non-carriers.

Structured PICO

Does an oral fat load unmask catalytic defects in normolipidemic carriers of the Asn291Ser mutation in the LPL gene compared to healthy controls?

Population

9 subjects: 3 unrelated normolipidemic Asn291Ser carriers, 5 healthy controls, and 1 subject with a 50% reduction in lipoprotein lipase (LPL) activity.

Intervention

Oral fat load

Comparator

Healthy controls (non-carriers) and a subject with a 50% reduction in LPL activity

Outcome

Postprandial chylomicron triglyceride and chylomicron retinyl palmitate peaks and area under response curvessurrogate

The Asn291Ser mutation in the LPL gene results in significant disturbances in postprandial chylomicron metabolism following an oral fat load, even in subjects with normal fasting lipid levels.

Cite This Study

Pimstone et al. (1996) studied this question.

synapsesocial.com/papers/6a82c07c0f52607ca18ae525 https://doi.org/10.1016/s0022-2275(20)39110-0

View Full Paper

Ask AI

Bookmark

Implication

Postprandial testing may detect functional LPL impairment in normolipidemic carriers; hypothesis-generating and requires prospective validation before clinical consideration.

A frequently occurring mutation in the lipoprotein lipase gene (Asn291Ser) results in altered postprandial chylomicron triglyceride and retinyl palmitate response in normolipidemic carriers.

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

A frequently occurring mutation in the lipoprotein lipase gene (Asn291Ser) results in altered postprandial chylomicron triglyceride and retinyl palmitate response in normolipidemic carriers.

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

Also Consider