Consumption of fructose-sweetened beverages for 10 weeks increases postprandial triacylglycerol and apolipoprotein-B concentrations in overweight and obese women

Dietary fructose consumption in the USA has increased by about 30% during the past three decades(1) and has coincided with a dramatic rise in the prevalence of obesity and its metabolic consequences(2,3). There is substantial evidence from studies conducted in animals and some in human subjects to indicate that high-fructose diets can promote the development of the metabolic syndrome(1,3,4). Fructose is primarily metabolised by the liver, where it is a highly lipogenic substrate(5). In animals, fructose consumption enhances hepatic de novo lipogenesis(6) and increases the secretion of apoB-containing VLDL particles(7). Similarly, in humans, consumption of a high-fructose diet can increase both fasting(8) and postprandial(9) plasma TAG concentrations relative to diets containing starch or glucose. High-fructose diets can promote insulin resistance in animals by directly interfering with hepatic insulin signalling(10–12); and the elevated postprandial TAG in response to fructose may further impair insulin sensitivity(13). Consistent with these effects, overfeeding human subjects with a high-fructose diet for 6 d not only led to increased de novo lipogenesis and plasma TAG, but also reduced hepatic insulin sensitivity(14). Unlike glucose, fructose does not stimulate insulin secretion, due to its hepatic metabolism and the low level of expression of the fructose transporter GLUT5 in pancreatic β-cells(15). The metabolic effects of long-term consumption of high-fructose diets have not been fully investigated in human subjects. In a short-term study in normal-weight women, we reported that consumption of fructose-sweetened beverages (providing 30% of total energy) with meals resulted in lowered postprandial glucose and insulin excursions, reduced 24 h circulating leptin concentrations relative to when the subjects consumed glucose-sweetened beverages, and produced sustained increases of postprandial plasma TAG(16). The present study was designed to investigate the effects of an isoenergetic 10-week intervention, in which 25% of daily energy requirements was provided as fructose-sweetened beverages, on fasting and postprandial glucose, insulin, TAG and plasma apoB concentrations.