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Postprandial decrease in HDL cholesterol and HDL apo A-I in normal subjects in relation to triglyceride metabolism.

T W De Bruin1, C B Brouwer, J A Gimpel

  • 1Department of Endocrinology, University Hospital, Utrecht, The Netherlands.

The American Journal of Physiology
|March 1, 1991
PubMed
Summary
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A fat-rich meal temporarily increases the risk of heart disease by lowering levels of beneficial HDL cholesterol and raising harmful particles. Hepatic lipase may play a key role in this postprandial lipoprotein metabolism.

Area of Science:

  • Lipid metabolism
  • Cardiovascular health
  • Nutritional science

Background:

  • Postprandial lipoprotein metabolism is crucial for understanding potentially atherogenic particle circulation.
  • Its influence on high-density lipoprotein (HDL) metabolism is complex and not fully understood.
  • Short-term changes after a fat load impact cardiovascular risk.

Purpose of the Study:

  • To investigate 24-hour changes in postprandial lipoprotein metabolism after an oral fat load.
  • To examine the relationship between retinyl palmitate (RP), apolipoprotein A-I (apo A-I), and apolipoprotein B levels.
  • To correlate these changes with postheparin lipolytic activities.

Main Methods:

  • Six healthy men underwent an oral retinyl palmitate (RP) fat tolerance test (98 g fat load).

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  • Measurements included plasma triglyceride (TG), RP, apo A-I, and apo B concentrations over 24 hours.
  • Postheparin lipolytic activities, including hepatic lipase, were assessed.

    • Main Results:

    • Triglyceride concentrations returned to baseline within 7 hours.
    • RP peaked at 4-5 hours, with remnants present up to 24 hours.
    • HDL cholesterol and HDL-associated apo A-I significantly decreased by 35% and 29%, respectively.
    • This decrease correlated with increased chylomicron remnants and TG-enriched HDL.
    • Hepatic lipase activity was linked to initial HDL cholesterol and peak TG remnant concentrations.

    Conclusions:

    • An oral fat load increases plasma atherogenic potential by reducing HDL cholesterol and apo A-I.
    • Hepatic lipase may be a key regulator in postprandial HDL and triglyceride metabolism.
    • Understanding these short-term changes is vital for cardiovascular risk assessment.