학술논문

The Dose-Response Effects of Consuming High Fructose Corn Syrup-Sweetened Beverages on Hepatic Lipid Content and Insulin Sensitivity in Young Adults
Document Type
article
Source
Nutrients. 14(8)
Subject
Biomedical and Clinical Sciences
Clinical Sciences
Diabetes
Clinical Trials and Supportive Activities
Nutrition
Liver Disease
Digestive Diseases
Clinical Research
Metabolic and endocrine
Oral and gastrointestinal
Beverages
Diabetes Mellitus
Type 2
Fructose
High Fructose Corn Syrup
Humans
Insulin Resistance
Lipids
Sugar-Sweetened Beverages
Young Adult
sugar-sweetened beverages
high-fructose corn syrup
liver fat
insulin sensitivity
lactate
Food Sciences
Nutrition and Dietetics
Clinical sciences
Nutrition and dietetics
Public health
Language
Abstract
Increased hepatic lipid content and decreased insulin sensitivity have critical roles in the development of cardiometabolic diseases. Therefore, our objective was to investigate the dose-response effects of consuming high fructose corn syrup (HFCS)-sweetened beverages for two weeks on hepatic lipid content and insulin sensitivity in young (18-40 years) adults (BMI 18-35 kg/m2). In a parallel, double-blinded study, participants consumed three beverages/day providing 0% (aspartame: n = 23), 10% (n = 18), 17.5% (n = 16), or 25% (n = 28) daily energy requirements from HFCS. Magnetic resonance imaging for hepatic lipid content and oral glucose tolerance tests (OGTT) were conducted during 3.5-day inpatient visits at baseline and again at the end of a 15-day intervention. During the 12 intervening outpatient days participants consumed their usual diets with their assigned beverages. Significant linear dose-response effects were observed for increases of hepatic lipid content (p = 0.015) and glucose and insulin AUCs during OGTT (both p = 0.0004), and for decreases in the Matsuda (p = 0.0087) and Predicted M (p = 0.0027) indices of insulin sensitivity. These dose-response effects strengthen the mechanistic evidence implicating consumption of HFCS-sweetened beverages as a contributor to the metabolic dysregulation that increases risk for nonalcoholic fatty liver disease and type 2 diabetes.