October 1, 1982European Journal of Clinical Investigation
Lipoprotein lipase activity of adipose tissue, skeletal muscle and post‐heparin plasma in primary endogenous hypertriglyceridaemia: relation to lipoprotein pattern and to obesity
Why the study?
Is lipoprotein lipase activity altered in adipose tissue, skeletal muscle, and post-heparin plasma of males with primary endogenous hypertriglyceridaemia compared to normolipidaemic males?
Population
135 males, comprising 65 with primary endogenous hypertriglyceridaemia and 70 with normal serum lipid levels.
Design
Case-control
Authors
Discussion
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Implication
Reduced adipose LPL activity may drive hypertriglyceridaemia; hypothesis-generating for LPL-targeted therapies in type 2b-5 phenotypes.
Structured PICO
Is lipoprotein lipase activity altered in adipose tissue, skeletal muscle, and post-heparin plasma of males with primary endogenous hypertriglyceridaemia compared to normolipidaemic males?
P
Population
135 males, comprising 65 with primary endogenous hypertriglyceridaemia (subgrouped into types 2b, 4, and 5) and 70 with normal serum lipid levels.
C
Comparator
70 males with normal serum lipid levels
O
Outcome
Lipoprotein lipase (LPL) activity in adipose tissue, skeletal muscle, and post-heparin plasmasurrogate
Low lipoprotein lipase activity in adipose tissue and skeletal muscle appears to be a crucial factor in the pathogenesis of hypertriglyceridaemia in nonobese subjects and those with type 5 hyperlipoproteinaemia.
Cite This Study
Taskinen et al. (1982) studied this question.