clearance of VLDL and intestinally derived chylomicrons [4]. An important consequence of slow clearance is the persistence in the circulation of VLDL, postprandial chylomicrons and partially metabolized remnant particles. Remnants include cholesterol-enriched intermediate-density lipoproteins that have been shown to confer high atherogenic risk in experimental animal models as well as in man [5]. Overproduction of VLDL, with increased secretion of TG and ApoB100, appears to be central in the etiology of increased plasma VLDL levels in patients with insulin resistance or T2DM [5]. Impairment of muscle glucose uptake and oxidation is a consequence of insulin resistance in muscle, while impairment of hepatic glucose production is a consequence of insulin resistance in liver. Finally, resistance to insulin's suppressive action in adipose tissue is accounting for the increased lipolysis in the insulin-resistant individual. Other research showed steps by which excess lipid depots could contribute to insulin resistance: 1 0 by altering supply (either in absolute terms or in particular anatomical locations, eg, portal vein to liver) or type of fatty acids, which then impact on insulin signaling or glucose metabolism in insulin-responsive tissues; 2 0 by increasing or decreasing secretion of humoral factors from adipocytes (adipokines) or liver (hepatokines) that enhance (eg, adiponectin, fibroblast growth factor 21) or inhibit (eg, Fetuin A) insulin signaling; 3 0 by attracting the invasion of cells, which release inflammatory cytokines (TNF) that impact on the insulin-signaling pathway in adjacent or distant tissue; 4 0 sequestering a favorable factor (25-hydroxyvitamin D [25OHD]) or by conversion of a circulating factor to a form with more adverse metabolic activity (eg, conversion of cortisone