apoB100 in the liver are constitutively synthesized, and that their secretion is regulated mainly by the availability of the core lipids (triglycerides and cholesteryl esters) that they deliver into the circulation. The assembly of chylomicrons is stimulated by the delivery of dietary lipids into the cells of the small intestinal villi. Both lipogenesis and the delivery of fatty acids (from either peripheral lipolysis of stored adipose tissue triglyceride or as components of TRLP remnant core lipids) can stimulate the assembly of VLDL in the liver. Microsomal triglyceride transfer protein (MTP) 14 plays a critical role in the transfer of lipoprotein lipids from the cytosol and/or endoplasmic reticulum membrane to nascent apoB. Indeed, absence of MTP results in the syndrome of abetalipoproteinemia and the absence of apoB lipoproteins. Recent studies indicating regulation of MTP gene expression by insulin, possibly via the transcriptional activity of sterol response element binding protein 1c (SREBP1c), suggests a molecular basis for the link between insulin resistance and increased VLDL secretion. 15 Also of note, a series of recent studies in cultured liver cells and in transgenic animals indicates that the level of apoE in the hepatocytes impacts the assembly and secretion of TRLP. 16, 17