Abstract
Background and Aims: Postprandial lipemia (PPL) is associated with atherosclerosis development and cardiovascular diseases. PCSK9 reduces plasma cholesterol by promoting LDLR degradation. We previously showed that PCSK9-deficiency reduced PPL by altering the intestinal chylomicron production and by increasing their hepatic catabolism. Our study aims: i) to assess the relative importance of hepatic or intestinal PCSK9 in PPL regulation ; ii) to assess the efficacy of an anti-PCSK9 monoclonal antibody on PPL in C57BL/6J and LDLR-/- mice ; iii) to determine whether PCSK9-deficiency also reduced PPL in insulinopenic streptozotocin(STZ)-induced diabetic mice.
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