Unlike chylomicron remnants, IDL has two competing metabolic fates: (1) uptake by the liver and (2) further processing to become LDL (Fig. 6).

Since IDL can be cleared by the liver or can be processed to become LDL, this branch point represents an important stage where LDL concentrations can be regulated. Inefficient clearance of IDL tends to lead to increased LDL production.

LDL is formed in the bloodstream through the catabolism of VLDL at the surface of blood vessels. In addition, VLDL is a triglyceride-rich lipoprotein, while LDL is cholesterol rich. The production of a cholesterol-rich lipoprotein from a triglyceride-rich lipoprotein occurs by selective removal of triglyceride from VLDL.

In summary, dietary fat is packaged into chylomicrons in the intestine. Dietary cholesterol is also packaged into chylomicrons, but a substantial fraction is delivered to the liver via chylomicron remnants. This cholesterol can then compete for the core of VLDL and appear in the bloodstream as cholesterol ester-enriched VLDL particles. Excess substrate in any form is converted into TG for export by the liver. For example, in some people, diets high in simple carbohydrates (e.g., fructose and sucrose) can lead to hypertriglyceridemia.

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