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Elevated Circulating Endocan Levels Are Associated with Increased Levels of Endothelial and Inflammation Factors in Postprandial Lipemia

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Background: Postprandial lipemia (PPL) causes endothelial dysfunction by causing endothelial damage to lipoproteins that remain rich in triglycerides. Endocan is a proteoglycan with increased tissue expression, endothelial activation, and neovascularization. The aim of the study was to examine circulating endocan levels in PPL subjects by considering the degree of PPL response according to a high-fat test meal. The other aim was to determine the association between endocan levels and endothelial and inflammatory factors. Method: Fifty-four hyperlipidemic subjects and 28 normolipidemic subjects consumed the high-fat meal. Endocan, sICAM-1, sVCAM-1, and VEGFA as endothelial factors and IL-6 and LFA-1α as inflammatory factors were evaluated. Results: Fasting serum endocan, VEGFA, sICAM-1, sVCAM-1 IL-6, and LFA-1α levels were increased in the PPL group compared to the control group. The PPL group was divided into tertiles based on mean AUC levels. Endocan levels in tertile 3 were at the highest and were increased significantly compared to tertiles 1 and 2. AUC and endocan levels were positively correlated with other endothelial and inflammation factors. ROC analysis showed endocan levels to be one of the highest values. Conclusions: Circulating endocan is seen at significantly higher levels and independently associated with endothelial and inflammatory factors in postprandial lipemia and dyslipidemia.
Title: Elevated Circulating Endocan Levels Are Associated with Increased Levels of Endothelial and Inflammation Factors in Postprandial Lipemia
Description:
Background: Postprandial lipemia (PPL) causes endothelial dysfunction by causing endothelial damage to lipoproteins that remain rich in triglycerides.
Endocan is a proteoglycan with increased tissue expression, endothelial activation, and neovascularization.
The aim of the study was to examine circulating endocan levels in PPL subjects by considering the degree of PPL response according to a high-fat test meal.
The other aim was to determine the association between endocan levels and endothelial and inflammatory factors.
Method: Fifty-four hyperlipidemic subjects and 28 normolipidemic subjects consumed the high-fat meal.
Endocan, sICAM-1, sVCAM-1, and VEGFA as endothelial factors and IL-6 and LFA-1α as inflammatory factors were evaluated.
Results: Fasting serum endocan, VEGFA, sICAM-1, sVCAM-1 IL-6, and LFA-1α levels were increased in the PPL group compared to the control group.
The PPL group was divided into tertiles based on mean AUC levels.
Endocan levels in tertile 3 were at the highest and were increased significantly compared to tertiles 1 and 2.
AUC and endocan levels were positively correlated with other endothelial and inflammation factors.
ROC analysis showed endocan levels to be one of the highest values.
Conclusions: Circulating endocan is seen at significantly higher levels and independently associated with endothelial and inflammatory factors in postprandial lipemia and dyslipidemia.

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