Role of the enterocyte in fructose-induced hypertriglyceridaemia

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Steenson, S., Umpleby, A. M., Lovegrove, J. A. orcid id iconORCID: https://orcid.org/0000-0001-7633-9455, Jackson, K. G. orcid id iconORCID: https://orcid.org/0000-0002-0070-3203 and Fielding, B. A. (2017) Role of the enterocyte in fructose-induced hypertriglyceridaemia. Nutrients, 9 (4). 349. ISSN 2072-6643 doi: 10.3390/nu9040349

Abstract/Summary

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.

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Item Type Article
URI https://reading-clone.eprints-hosting.org/id/eprint/69986
Identification Number/DOI 10.3390/nu9040349
Refereed Yes
Divisions Interdisciplinary centres and themes > Institute for Cardiovascular and Metabolic Research (ICMR)
Life Sciences > School of Chemistry, Food and Pharmacy > Department of Food and Nutritional Sciences > Human Nutrition Research Group
Publisher MDPI
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