Serum triglyceride concentrations are composed of two fractions. One fraction is composed of the endogenously produced very low density lipoproteins (VLDL) that are synthesised in the liver by the process of de novo lipogenesis. This process is active postprandially and the VLDL are subsequently exported to the peripheral tissues for oxidation or storage. Alternatively, another fraction is derived from the intestinal absorption of fatty acids, that are packaged into chylomicrons and enter circulation via the lymphatic system. Postprandially serum triglycerides increase because fatty acids are absorbed from the gut and because insulin stimulates the synthesis of fatty acids in the liver. Triglyceride measurements do not differentiate the two fractions and so the origin of the triglycerides is not know. However, researchers can administer vitamin A with a fat test meal which is then incorporated into chylomicrons, and this can be measured to estimate triglycerides of intestinal origin.
Researchers have used this method to determine the effects of fructose on a high fat meal in healthy volunteers. Eleven subjects were fed a 40g fat load or a 40g fat load with an additional 50g of fructose. Vitamin A was used to label the intestinal lipoproteins, and the retinyl palmitate concentration of the Sf>400 and Sf20-400 fractions in plasma was used to differentiate the intestinal triglycerides from the endogenously produced triglycerides. The results showed that addition of fructose to a fat load increased postprandial concentrations of serum triglycerides, with higher concentrations of triglycerides and retinyl palmitate in the Sf>400 fraction, indicative of mainly the chylomicron fraction. However, the serum triglyceride fraction Sf20-400, indicative of VLDL, was not different between the two test meals. These results suggest that fructose can increase the concentrations of serum lipids as reported in other studies.
However, the increase in triglycerides was caused by an increase in the chylomicron fraction (Sf>400) and not through increases in VLDL (Sf20-400). Because fructokinase, the enzyme that allows fructose to feed into glycolysis, is not present in the small intestine, it must be assumed that the increase in chylomicron concentration is not due to increase production of triglycerides in the enterocytes. Therefore it is likely that fructose ingestion causes an increase de novo lipogenesis in the liver, with a subsequent increase in VLDL. The endogenously produced triglycerides may then have subsequently competed with the chylomicrons for a common catabolic pathway, thus preventing the removal of the chylomicrons from circulation. Raised levels of triglycerides are a risk factor for cardiovascular disease, and so high fructose diets should be considered a contributory factor.
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