Abstract

Nonalcoholic fatty liver disease (NAFLD) is now thought to be the most common liver disease worldwide. Cardiovascular complications are a leading cause of mortality in NAFLD. Fructose, a common nutrient in the westernized diet, has been reported to be associated with increased cardiovascular risk, but its impact on adolescents with NAFLD is not well understood. We designed a 4-week randomized, controlled, double-blinded beverage intervention study. Twenty-four overweight Hispanic-American adolescents who had hepatic fat >8% on imaging and who were regular consumers of sweet beverages were enrolled and randomized to calorie-matched study-provided fructose only or glucose only beverages. After 4 weeks, there was no significant change in hepatic fat or body weight in either group. In the glucose beverage group there was significantly improved adipose insulin sensitivity, high sensitivity C-reactive protein (hs-CRP), and low-density lipoprotein (LDL) oxidation. These findings demonstrate that reduction of fructose improves several important factors related to cardiovascular disease despite a lack of measurable improvement in hepatic steatosis. Reducing dietary fructose may be an effective intervention to blunt atherosclerosis progression among NAFLD patients and should be evaluated in longer term clinical trials.

Highlights

  • Nonalcoholic fatty liver disease (NAFLD) has become a major cause of chronic liver disease worldwide

  • In a calorie-matched, randomized, controlled study, we examined whether hepatic steatosis and associated cardiovascular risk factors would be improved after 4 weeks of substitution of usual high fructose containing beverages with study-provided glucose only beverages

  • We found that fructose reduction through replacing usual sweet beverages with glucose-only beverages resulted in an improved cardiometabolic profile, including increased insulin sensitivity, reduced high sensitivity C-reactive protein (hs-CRP), fewer large Very low density lipoprotein (VLDL) particles and fewer oxidized low-density lipoprotein (LDL)

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Summary

Introduction

Nonalcoholic fatty liver disease (NAFLD) has become a major cause of chronic liver disease worldwide. Global NAFLD prevalence estimates range from 2.8% to 46%, with increased risk in patients with type 2 diabetes mellitus [1,2,3]. The rising number of children with NAFLD is of considerable public health concern because they may have a more aggressive, earlier onset form of the disease. Estimates of NAFLD in the general pediatric population range from 3% to 11% [4,5,6]. NAFLD can lead to end stage liver disease and is closely associated with cardiovascular disease (CVD) [8,9,10].

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