Postprandial adipose tissue lipoprotein lipase activity in primary hypertriglyceridemia

Area of Science:

• Lipid Metabolism
• Enzymology
• Human Physiology

Background:

• Primary hypertriglyceridemia is characterized by elevated triglyceride levels.
• Previous studies indicated variable fasting adipose tissue lipoprotein lipase (AT-LPL) activity.
• Postprandial AT-LPL activity in hypertriglyceridemia remains largely uncharacterized.

Purpose of the Study:

• To investigate and compare fasting and postprandial AT-LPL activity in subjects with primary hypertriglyceridemia versus healthy controls.
• To explore potential differences in AT-LPL activity across various genetic subtypes of hypertriglyceridemia.
• To examine the relationship between AT-LPL activity, fasting enzyme levels, and postprandial triglyceride response.

Main Methods:

• Measurement of heparin-elutable AT-LPL activity from adipose tissue biopsies.
• Analysis of enzyme activity in acetone-ether tissue powder extracts.
• Assessment of AT-LPL activity following a high-carbohydrate meal in both normal and hypertriglyceridemic subjects.

Main Results:

• Fasting and postprandial AT-LPL activity were similar in primary hypertriglyceridemia and normal subjects.
• No significant differences in AT-LPL activity were observed among familial hypertriglyceridemia, familial combined hyperlipidemia, and undiagnosed hypertriglyceridemia groups.
• A significant inverse correlation was found between fasting AT-LPL levels and the change in activity after feeding in both groups.
• In normal subjects, postprandial triglyceride response inversely correlated with postprandial AT-LPL activity change.
• Patients with primary lipoprotein lipase deficiency exhibited markedly reduced fasting AT-LPL activity, near zero post-feeding.

Conclusions:

• Adipose tissue lipoprotein lipase activity is not significantly impaired in the fasting or postprandial state in primary hypertriglyceridemia.
• The measured AT-LPL activity appears functional, as evidenced by its near absence in primary lipoprotein lipase deficiency.
• These findings suggest that other factors may contribute to the hypertriglyceridemia phenotype beyond AT-LPL activity levels.