Relevance of liver fat to the impact of dietary extrinsic sugars on lipid metabolism

Abstract

In contrast to the decline in mortality from many non-infectious, chronic diseases in the UK, death from liver disease has increased exponentially in men and women over the past 40 years. This is primarily because of the over consumption of alcohol, but also the increased prevalence of obesity, which is linked to early pathology through the accumulation of liver fat. Supra-physiological intakes of fructose-containing sugar can produce acute, adverse effects on lipid metabolism, and deliver excess energy that increases bodyweight and the deposition of fat in sites other than adipose tissue, including the liver. This review addresses the variable metabolic origins of liver fat, and the key importance of postprandial lipid metabolism in this respect. The effects of supra-physiological intakes of sugar are also considered in context of the real world and established threshold for the adverse effects of sugar on cardio-metabolic risk factors. The review concludes that while the average intake of sugar in the UK falls well below this critical threshold, intakes in subgroups of adults, and especially adolescents, may be cause for concern. There is also evidence to suggest that raised liver fat, acquired, in part, through an impaired removal of postprandial lipaemia, can increase sensitivity to the adverse effects of sugar at all ages.

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

“…While postprandial responses were not measured in our study, the high sugar diet increased VLDL 1 in controls, and serum apo C-III in NAFLD, an apoprotein with roles in the assembly of VLDL 1 in the liver and inhibition of LPL [37]. These effects are consistent with dietary free sugars impairing the clearance of plasma TAG in the postprandial phase [35,36].…”

“…However, since visceral fat was not different between groups and unaffected by the diets in the present study, this suggests that the relatively greater contribution of splanchnic-derived NEFAs to VLDL 1 and VLDL 2 -TAG production on the high sugars diet in NAFLD relative to controls, came from hepatic TAG storage pools. This possibility introduces the established effect of dietary sugars in augmenting post-prandial lipaemia [35], and highlights the importance of postprandial TAG as a potential source of lipid for the accumulation of liver fat [36]. While postprandial responses were not measured in our study, the high sugar diet increased VLDL 1 in controls, and serum apo C-III in NAFLD, an apoprotein with roles in the assembly of VLDL 1 in the liver and inhibition of LPL [37].…”

Sugar and metabolic health

“…Syrups are particularly confusing, the demonizing of fructose in the form of HFCS consumption in the US [38] , may lead the European public to perhaps believe they are safer.…”

Adverse effects of fructose on cardiometabolic risk factors and hepatic lipid metabolism in subjects with abdominal obesity

“…Numerous risk factors for CVD have been identified, including a number of nutritional factors. Dietary sugars have come under scrutiny because of epidemiologic studies suggesting a possible link between sugar‐sweetened beverages and CVD risk factors such as type 2 diabetes, obesity, hypertension and dyslipidemia . In addition, overconsumption of dietary sugars has been linked to nonalcoholic fatty liver disease (NAFLD).…”