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Decreased apolipoprotein E and VLDL receptors cause lipidemia in nephrotic syndrome
Author(s) -
Wang Limin,
Walzem Rosemary L,
Kaysen George
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.694.16
Subject(s) - very low density lipoprotein , medicine , endocrinology , lipoprotein lipase , apolipoprotein b , chemistry , apolipoprotein e , hyperlipidemia , lipoprotein , nephrotic syndrome , lipolysis , triglyceride , receptor , catabolism , biology , cholesterol , metabolism , adipose tissue , disease , diabetes mellitus
Hyperlipidemia in nephrotic syndrome (NS) is due to decreased clearance of triglyceride rich lipoproteins (TGLs). Lipoprotein lipase (LPL) hydrolyzes plasma TG, promotes the binding and catabolism of TGLs. Apolipoprotein E (apo E) facilitates binding by TGLs both to their receptor and LPL. A reduced plasma LpL level and reduced VLDL apo E were found in nephrotic rats. It is unknown whether low levels of LPL and/or VLDL apoE may contribute to the defective clearance. Lipoprotein particle size measured by Microtrac, showed no significant difference in nephrotic VLDL compared with control one. This finding indicated that the increased lipids in NS are due to increased particles accumulation in plasma instead of defective TGLs lipolysis via LpL. To study whether this accumulation is from decreased clearance and/or uptake by cells and organs, heart perfusion study demonstrated a significant decrease of VLDL uptake in NS heart. Endothelial cell VLDL uptake using fluorescent labeling technique showed a significant decreased cell uptake VLDL in NS compared with control. However, two groups had a similar increase when adding exogenous LpL. ApoE significantly increased VLDL cell uptake in NS compared with control at low concentration, but not at high concentration. Further, Western showed a significant decreased VLDL receptor in NS heart. These findings indicate that decreased LpL in nephrotic is not the major cause of defective VLDL clearance, decreased apoE and VLDL receptor contribute to the defect. The study was supported by the Department of Veteran's Affairs.