Lipoprotein lipase in plasma after an oral fat load: relation to free fatty acids.
Key result
An oral fat load doubled mean LPL activity at 6 hours (P<0.01), and the AUC for LPL correlated significantly with the AUC for linoleic free fatty acids (r=0.40, P<0.05).
Why the study?
Does an oral fat load affect plasma LPL activity and free fatty acid levels in humans?
Population
Humans subjected to an oral fat tolerance test
Comparison
Oral fat tolerance test of a mixed-meal type vs Baseline measurements before fat load
Design
Cohort
Follow-up
12 hours
Authors
Discussion
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Implication
Supports fatty acid control of endothelial LPL; hypothesis-generating and requires prospective validation before clinical consideration.
Study Design
Type
Observational
Structured PICO
Does an oral fat load affect plasma LPL activity and free fatty acid levels in humans?
P
Population
Humans subjected to an oral fat tolerance test
I
Intervention
Oral fat tolerance test of a mixed-meal type (soybean oil source)
C
Comparator
Baseline measurements before fat load
O
Outcome
Plasma LPL activity, triglycerides, and free fatty acids (total and linoleic) over a 12-h periodsurrogate
Main Result
Effect estimate: r = 0.40
p-value: p=<0.05
Postprandial plasma LPL activity parallels and correlates with linoleic free fatty acids, supporting the hypothesis of fatty acid control of endothelial LPL.
Cite This Study
Karpe et al. (1992) reported an observational. Oral fat load (soybean oil) vs. Baseline was evaluated on Correlation between AUC for plasma LPL and AUC for 18:2 FFA (r = 0.40, p=<0.05). An oral fat load doubled mean LPL activity at 6 hours (P<0.01), and the AUC for LPL correlated significantly with the AUC for linoleic free fatty acids (r=0.40, P<0.05).