Abstract
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.
Highlights
Cardiovascular disease (CVD) remains the primary cause of death from non-communicable diseases globally, according to the World Health Organisation [1]
These findings clearly demonstrate that fructose and glucose have differential effects on intestinal lipoprotein particle production and their subsequent metabolism
The importance of intestinal lipid metabolism has gained widespread appreciation in recent years, including the role of enterocyte lipid droplets (LD) and CM particle over-production as determinants of HTG, which may impact on CVD risk
Summary
Cardiovascular disease (CVD) remains the primary cause of death from non-communicable diseases globally, according to the World Health Organisation [1]. Many dietary studies in bothformation animals and humans have investigated effects of fructose on occur without contribute to atherosclerotic plaque [21,22,23], and thatthe this process may the metabolism of hepatic very‐low density lipoprotein (VLDL), as a determinant of total plasma TG particle oxidation [24]. The amount of energy differed between test meals, and there was a lack of starch and fibre In spite of these methodological issues, these novel findings demonstrate the capacity of human small intestine enterocytes to synthesise de novo FA from fructose, which may make a more meaningful contribution to post-prandial HTG than previously appreciated
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