Consuming Sucrose- or HFCS-sweetened Beverages Increases Hepatic Lipid and Decreases Insulin Sensitivity in Adults

Abstract

Context Studies in rodents and humans suggest that high fructose corn syrup (HFCS)-sweetened diets promote greater metabolic dysfunction than sucrose-sweetened diets. Objective To compare the effects of consuming sucrose-sweetened beverage (-SB), HFCS-SB, or a control beverage sweetened with aspartame on metabolic outcomes in humans. Design A parallel, double-blinded, NIH-funded study. Setting Experimental procedures were conducted during 3.5 days of inpatient residence with controlled feeding at a research clinic before (baseline) and after a 12-day outpatient intervention period. Participants 75 adults (18-40 years) were assigned to beverage groups matched for sex, BMI (18-35kg/m 2), fasting triglyceride, lipoprotein and insulin concentrations. Intervention 3 servings/day of sucrose- or HFCS-SB providing 25% of energy requirement or aspartame-SB, consumed for 16 days. Main Outcome Measures %Hepatic lipid, Matsuda insulin sensitivity index (ISI), and Predicted M ISI. Results Sucrose-SB increased %hepatic lipid (absolute change: 0.6±0.2%) compared with aspartame-SB (-0.2±0.2%, P<0.05) and compared with baseline (P<0.001). HFCS-SB increased %hepatic lipid compared with baseline (0.4±0.2%, P<0.05). Compared with aspartame-SB, Matsuda ISI decreased after consumption of HFCS- (P<0.01) and sucrose-SB (P<0.01), and Predicted M ISI decreased after consumption of HFCS-SB (P<0.05). Sucrose- and HFCS-SB increased plasma concentrations of lipids, lipoproteins, and uric acid compared with aspartame-SB. No outcomes were differentially affected by sucrose- compared with HFCS-SB. Beverage group effects remained significant when analyses were adjusted for changes in body weight. Conclusions Consumption of both sucrose- and HFCS-SB induced detrimental changes in hepatic lipid, insulin sensitivity, and circulating lipids, lipoproteins and uric acid in 2 weeks.

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Ethnic disparities attributed to the manifestation in and response to type 2 diabetes: insights from metabolomics

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