title: The regulation of ApoB metabolism by insulin.
abstract: 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.
authors.affiliation: Division of Endocrinology, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
authors.forename: Mary E
authors.initials: ME
authors.lastname: Haas
authors.forename: Alan D
authors.initials: AD
authors.lastname: Attie
authors.forename: Sudha B
authors.initials: SB
authors.lastname: Biddinger
mesh_terms: D000818:Animals; D001055:Apolipoproteins B / Q000378:metabolism*; D002318:Cardiovascular Diseases / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D007333:Insulin Resistance / Q000502:physiology; D008079:Lipoproteins, VLDL / Q000378:metabolism
chemical_list: D001055:Apolipoproteins B; D007328:Insulin; D008079:Lipoproteins, VLDL
keywords: apolipoprotein B; cardiovascular disease; diabetes; insulin; selective insulin resistance; very low-density lipoprotein (VLDL)