Plasma lipoproteins levels are important because alteration in the ratios of the various fractions can alter the risk of developing cardiovascular disease. In particular, raised levels of low density lipoprotein (LDL) and very low density liporprotein (VLDL) are often cited as detrimental. Very low density lipoprotein transports most of the triglycerides in humans and is split into VLDL1 (Sf 60-400) and the smaller VLDL2 (Sf 20-60) subfractions. The liver can regulate the levels of VLDL1 and VLDL2 subfractions. The VLDL2 subfractions have a reduced triglyceride content and instead are enriched in cholesteryl ester as well as having a lower ratio of apolipoprotein E and apolipoprotein C to apolipoprotein B. Some evidence suggests that increased concentrations of VLDL1 can give rise to increased levels of small LDL particles, which are though to increase risk of cardiovascular disease to a greater extent than the larger more buoyant LDL particles.
The interaction between food and lipoproteins is complex, and not fully understood, but the traditional model that suggests that saturated fat and cholesterol are detrimental to plasma lipoproteins overly simplistic. Instead research is accumulating that catalogues the beneficial or detrimental effects of a wide variety of foods on the various plasma lipoprotein particles levels. For example, research has investigated the coffee diterpene cafestol, present in coffee on the plasma levels of VLDL1 and VLDL2 in humans. Eight healthy men were fed 75 mg of cafestol for 2 weeks while levels of plasma lipoproteins were measured. Cafestol caused a significant 31% increase in plasma triglycerides which was caused mainly by an increase in the VLDL1 subfraction. The authors concluded that this change occurred because of an 80% increase VLDL1 apolipoprotein B production in the liver. At the same time, VLDL2 subfraction became enriched with cholesteryl ester at the expense of triglycerides.
The cafestol administered in this study was equivalent to the amount found in around 15 cups of unfiltered coffee and so was on the very high side of normal consumption. This levels of cafestol increased VLDL1 apolipoprotein B triglyceride levels but did not alter their composition. However. it did alter the composition of the VLDL2 subfraction by enriching it with cholesteryl ester. This cholesterol may originate from cholesterol in the bile, because cafestol has been shown to inhibit bile synthesis in mice. The cholesterol may therefore become available in the liver because of reduced bile synthesis and subsequently be packaged into VLDL2 particles. The authors suggest that cafestol might increase VLDL1 apolipoprotein B levels by increasing the synthesis inside liver cells. These results are more evidence of the complex interaction between food and plasma lipoprotein levels and demonstrate that diet heart models based on single macronutrients are outdated.
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