摘要：Dietary fructose has been linked to an increased post-prandial triglyceride (TG) level; which is an established independent risk factor for cardiovascular disease. Although much research has focused on the effects of fructose consumption on liver-derived very-low density lipoprotein (VLDL); emerging evidence also suggests that fructose may raise post-prandial TG levels by affecting the metabolism of enterocytes of the small intestine. Enterocytes have become well recognised for their ability to transiently store lipids following a meal and to thus control post-prandial TG levels according to the rate of chylomicron (CM) lipoprotein synthesis and secretion. The influence of fructose consumption on several aspects of enterocyte lipid metabolism are discussed; including de novo lipogenesis; apolipoprotein B48 and CM-TG production; based on the findings of animal and human isotopic tracer studies. Methodological issues affecting the interpretation of fructose studies conducted to date are highlighted; including the accurate separation of CM and VLDL. Although the available evidence to date is limited; disruption of enterocyte lipid metabolism may make a meaningful contribution to the hypertriglyceridaemia often associated with fructose consumption.
关键词：fructose; chylomicron; very low-density lipoprotein; triglyceride-rich lipoproteins; cardiovascular disease; de novo lipogenesis; post-prandial; apoB48; gluconeogenesis; glucagon-like peptide fructose ; chylomicron ; very low-density lipoprotein ; triglyceride-rich lipoproteins ; cardiovascular disease ; de novo lipogenesis ; post-prandial ; apoB48 ; gluconeogenesis ; glucagon-like peptide
