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In case of low TG availability, the liver secretes mostly VLDL1 and IDL as TG-rich and TG-poor lipoprotein particles.
Hypertriglyceridemia, mostly due to excessive production of large, buoyant VLDL1 particles, low HDL-C, preponderance of the small dense LDL particles subclass and prolonged postprandial lipemia have been briefly reviewed, and the major role of insulin resistance has been emphasized.
VLDL3: VLDL3 is the densest VLDL sub-fraction, and confers a greater risk factor for heart disease than both VLDL1 and VLDL2.
An approximate 50% decrease in VLDL1 apoB production (P < .05) is observed when normal subjects are given an insulin infusion, but it is not replicated when the same infusion is given to patients with type 2 diabetes.
Early alterations in the postprandial VLDL1 apoB-100 and apoB-48 metabolism in men with strong heredity for type 2 diabetes.
Each lipid is involved in a tightly linked metabolic pathway,  beginning with the hepatic production and secretion of VLDL1, an abnormally large VLDL molecule (see Figure 3, below).
VLDL1 leads to the generation of LDL molecules that ultimately are smaller or thicker than the typical, more buoyant LDL, which binds with the LDL receptor.
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