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Quantitation of Endothelial Cell Adhesiveness In Vitro
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Endothelial cell adhesion molecules in healthy adults during acute hyperhomocysteinemia and mild hypertriglyceridemia

M A Mansoor1, I Seljeflot, H Arnesen

  • 1Division of Medical Biochemistry, Rogaland Central Hospital, 4068 Stavanger, Norway. azam@ext.sir.no

Clinical Biochemistry
|April 17, 2004
PubMed

Insights

Concurrent hyperhomocysteinemia and hypertriglyceridemia activate endothelial inflammation in healthy subjects. This study shows increased cellular adhesion molecules, indicating endothelial dysfunction from combined metabolic challenges.

Area of Science:

  • Cardiovascular Research
  • Metabolic Syndrome
  • Endothelial Biology

Background:

  • Hyperhomocysteinemia and hypertriglyceridemia are independent risk factors for atherosclerotic disease.
  • Atherogenesis involves inflammatory processes and endothelial dysfunction.

Purpose of the Study:

  • To investigate if combined acute hyperhomocysteinemia and mild hypertriglyceridemia elevate circulatory cellular adhesion molecules in healthy individuals.

Main Methods:

  • Twelve healthy volunteers underwent loading with methionine, fat, both, or water (control).
  • Plasma total homocysteine, serum triglycerides, cellular adhesion molecules (CAMs), and nitrate concentrations were measured over 6 hours.
  • Wash-out periods of at least one week separated each loading condition.

Main Results:

  • Methionine and methionine + fat loading significantly altered plasma homocysteine levels compared to controls.
  • Fat and combined loading synergistically increased triglyceride levels.
  • Concurrent loading led to significant increases in P-selectin, E-selectin, and VCAM-1 levels, indicating endothelial activation.
  • Nitrate levels decreased, with a more pronounced reduction after combined loading.

Conclusions:

  • Transient, concurrent hyperhomocysteinemia and mild hypertriglyceridemia induce inflammatory activation of the endothelium.
  • These findings suggest a combined metabolic insult contributes to endothelial dysfunction and atherogenesis.
Abstract

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