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Clin Sci (Lond). 2017 Oct 17;131(21):2561-2573. doi: 10.1042/CS20171208. Print 2017 Nov 1.

Impact of liver fat on the differential partitioning of hepatic triacylglycerol into VLDL subclasses on high and low sugar diets.

Author information

1
Faculty of Health and Medical Sciences, University of Surrey, Guildford, U.K.
2
Faculty of Health Sciences, University Sultan Zainal Abidin, 21300 Kuala Nerus,Terengganu, Malaysia.
3
Hugh Sinclair Unit of Human Nutrition and Institute for Cardiovascular and Metabolic Research, University of Reading, Reading, U.K.
4
Diabetes Modelling Group, Institute of Metabolic Science, University of Cambridge, Cambridge, U.K.
5
Metabolic and Molecular Imaging Group, MRC Clinical Sciences Centre, Imperial College London, Hammersmith Hospital, London, U.K.
6
Research Centre for Optimal Health, Department of Life Sciences, University of Westminister, London, U.K.
7
Nutrition and Dietetic Research Group, Section of Investigative Medicine, Division of Diabetes, Endocrinology and Metabolism, Imperial College London, U.K.
8
Faculty of Health and Medical Sciences, University of Surrey, Guildford, U.K. b.griffin@surrey.ac.uk.

Abstract

Dietary sugars are linked to the development of non-alcoholic fatty liver disease (NAFLD) and dyslipidaemia, but it is unknown if NAFLD itself influences the effects of sugars on plasma lipoproteins. To study this further, men with NAFLD (n = 11) and low liver fat 'controls' (n = 14) were fed two iso-energetic diets, high or low in sugars (26% or 6% total energy) for 12 weeks, in a randomised, cross-over design. Fasting plasma lipid and lipoprotein kinetics were measured after each diet by stable isotope trace-labelling.There were significant differences in the production and catabolic rates of VLDL subclasses between men with NAFLD and controls, in response to the high and low sugar diets. Men with NAFLD had higher plasma concentrations of VLDL1-triacylglycerol (TAG) after the high (P<0.02) and low sugar (P<0.0002) diets, a lower VLDL1-TAG fractional catabolic rate after the high sugar diet (P<0.01), and a higher VLDL1-TAG production rate after the low sugar diet (P<0.01), relative to controls. An effect of the high sugar diet, was to channel hepatic TAG into a higher production of VLDL1-TAG (P<0.02) in the controls, but in contrast, a higher production of VLDL2-TAG (P<0.05) in NAFLD. These dietary effects on VLDL subclass kinetics could be explained, in part, by differences in the contribution of fatty acids from intra-hepatic stores, and de novo lipogenesis. The present study provides new evidence that liver fat accumulation leads to a differential partitioning of hepatic TAG into large and small VLDL subclasses, in response to high and low intakes of sugars.

KEYWORDS:

Sugar; non alcoholic fatty liver disease; plasma lipoproteins; triglycerides

PMID:
28923880
DOI:
10.1042/CS20171208
[Indexed for MEDLINE]
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