%0 Journal Article
%T Role of the Enterocyte in Fructose-Induced Hypertriglyceridaemia
%A A. Margot Umpleby
%A Barbara A. Fielding
%A Julie A. Lovegrove
%A Kim G. Jackson
%A Simon Steenson
%J Archive of "Nutrients".
%D 2017
%R 10.3390/nu9040349
%X 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
%K fructose
%K chylomicron
%K very low-density lipoprotein
%K triglyceride-rich lipoproteins
%K cardiovascular disease
%K de novo lipogenesis
%K post-prandial
%K apoB48
%K gluconeogenesis
%K glucagon-like peptide
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5409688/