Journal
TRENDS IN ENDOCRINOLOGY AND METABOLISM
Volume 24, Issue 8, Pages 391-397Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tem.2013.04.001
Keywords
apolipoprotein B; insulin; diabetes; very low-density lipoprotein (VLDL); cardiovascular disease; selective insulin resistance
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Funding
- NHLBI NIH HHS [R01 HL109650] Funding Source: Medline
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The leading cause of death in diabetic patients is cardiovascular disease. Apolipoprotein B (ApoB)-containing lipoprotein particles, which are secreted and cleared by the liver, are essential for the development of atherosclerosis. Insulin plays a key role in the regulation of ApoB. Insulin decreases ApoB secretion by promoting ApoB degradation in the hepatocyte. In parallel, insulin promotes clearance of circulating ApoB particles by the liver via the low-density lipoprotein receptor (LDLR), LDLR-related protein 1 (LRP1), and heparan sulfate proteoglycans (HSPGs). Consequently, the insulin-resistant state of type 2 diabetes (T2D) is associated with increased secretion and decreased clearance of ApoB. Here, we review the mechanisms by which insulin controls the secretion and uptake of ApoB in normal and diabetic livers.
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