Serum levels of pigment epithelium-derived factor, a novel marker of insulin resistance, are independently associated with fasting apolipoprotein B48 levels in humans
文摘

Objectives

Fasting apolipoprotein B48 (apoB48) levels are associated with postprandial hyperlipidemia and carotid artery intima-media thickness (IMT), one of the markers of metabolic derangements and atherosclerosis, respectively. However, it remains unknown whether fasting serum levels of apoB48 are independently correlated with insulin resistance and vascular inflammation in humans.

Design and methods

The study involved 315 consecutive outpatients in our hospital (218 males and 97 females) with a mean age of 62.0 ¡À 9.2. We examined which anthropometric, metabolic and inflammatory variables, including serum levels of pigment epithelium-derived factor (PEDF), a novel marker of insulin resistance were independently associated with fasting apoB48. Moreover, we investigated whether fasting apoB48 levels were correlated with atherosclerotic plaque inflammation evaluated by [18F]-fluorodeoxyglucose positron emission tomography (FDG-PET). Carotid [18F]-FDG uptake, an index of vascular inflammation within the atherosclerotic plaques, was measured as blood-normalized standardized uptake value, known as the target-to-background ratio (TBR).

Results

Mean serum levels of apoB48, PEDF, carotid IMT and TBR values were 2.77 ¡À 0.21 ¦Ìg/mL, 13.45 ¡À 1.03 ¦Ìg/mL, 0.71 ¡À 0.15 mm, and 1.43 ¡À 0.21, respectively. Univariate analysis revealed that apoB48 levels were weakly, but not significantly associated with TBR (p = 0.057). In multiple stepwise regression analysis, triglycerides (p < 0.001), male (p = 0.039), age (inversely, p = 0.010), uric acid (p = 0.007), medication for diabetes (p = 0.029), and PEDF (p = 0.049) were independently correlated to fasting apoB48 levels (R2 = 0.371).

Conclusions

The present study reveals that serum levels of PEDF are independently associated with fasting apoB48 levels, suggesting that PEDF level is a novel biomarker that could reflect postprandial hyperlipidemia in humans.

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