Abstract
ApoCIII and triglyceride (TG)-rich lipoproteins (TRL), particularly, large TG-rich lipoproteins particles, have been described as important mediators of cardiovascular disease (CVD) risk. The effects of sustained consumption of dietary fructose compared with those of sustained glucose consumption on circulating apoCIII and large TRL particles have not been reported. We measured apoCIII concentrations and the TG and cholesterol content of lipoprotein subfractions separated by size in fasting and postprandial plasma collected from men and women (age: 54 ± 8 years) before and after they consumed glucose- or fructose-sweetened beverages for 10 weeks. The subjects consuming fructose exhibited higher fasting and postprandial plasma apoCIII concentrations than the subjects consuming glucose (p < 0.05 for both). They also had higher concentrations of postprandial TG in all TRL subfractions (p < 0.05, effect of sugar), with the highest increases occurring in the largest TRL particles (p < 0.0001 for fructose linear trend). Compared to glucose consumption, fructose consumption increased postprandial TG in low-density lipoprotein (LDL) particles (p < 0.05, effect of sugar), especially in the smaller particles (p < 0.0001 for fructose linear trend). The increases of both postprandial apoCIII and TG in large TRL subfractions were associated with fructose-induced increases of fasting cholesterol in the smaller LDL particles. In conclusion, 10 weeks of fructose consumption increased the circulating apoCIII and postprandial concentrations of large TRL particles compared with glucose consumption.
Highlights
The incidence and prevalence of undesirable health outcomes including obesity, type-2 diabetes, cardiovascular disease (CVD), and metabolic syndrome are increasing in developing and developed countries alike, with CVD being the number one cause of death globally [1]
We have previously reported that the two sugars had highly significant and opposite effects on circulating insulin, with glucose consumption increasing, and fructose consumption decreasing 24 h area under the curve (AUC) and post-meal insulin responses [29]
Cell culture experiments showed apoCIII expression is induced by glucose via hepatocyte nuclear factor 4 alpha (HNF-4α) and carbohydrate-responsive element-binding protein (ChREBP) [30] and is reduced by insulin via Forkhead Box O1 (FOXO1) [28]
Summary
The incidence and prevalence of undesirable health outcomes including obesity, type-2 diabetes, cardiovascular disease (CVD), and metabolic syndrome are increasing in developing and developed countries alike, with CVD being the number one cause of death globally [1]. Dietary habits affect cardiometabolic risk [2], but we lack a full understanding of how dietary patterns influence the development of undesirable lipid profiles that lead to metabolic diseases. Understanding the mechanisms that link specific dietary components and patterns to atherogenic dyslipidemia will promote the implementation of dietary policies to reduce CVD risk. Despite comparable weight gain in both groups, fructose consumption promoted lipid dysregulation, while glucose consumption did not [3]. The consumption of fructose increased the circulating concentrations of postprandial triglycerides (TG), remnant-like particle lipoprotein (RLP)-TG, and RLP-cholesterol (chol), as well as those of fasting total chol, low-density lipoprotein (LDL)-chol, apolipoprotein B (apoB), small dense LDL-chol (sdLDL-chol), and oxidized LDL [3]. Subjects consuming fructose exhibited increased postprandial hepatic de novo lipogenesis (DNL) and decreased insulin sensitivity compared with subjects consuming glucose [3]
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