Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans

Abstract

Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance. To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose-or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Although both groups exhibited similar weight gain during the intervention, visceral adipose volume was significantly increased only in subjects consuming fructose. Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption. In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle-triglyceride and -cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults. IntroductionStudies investigating the effects of fructose consumption in humans and animals have been comprehensively reviewed (1-4), and while strong evidence exists that consumption of diets high in fructose results in increased de novo lipogenesis (DNL), dyslipidemia, insulin resistance, and obesity in animals, direct experimental evidence that consumption of fructose promotes DNL, dyslipidemia, insulin resistance, glucose intolerance, and obesity in humans is lacking. Thus, we have investigated and compared the biological effects of the 2 major simple sugars in the diet, glucose and fructose, on BW and regional fat deposition and on indices of lipid and carbohydrate metabolism in older, overweight and obese men and women.We sought to answer the following questions: (a) Does consumption of fructose with an ad libitum diet promote greater BW gain and have differential effects on regional adipose deposition and adipose gene expression compared with consumption of glucose with an ad libitum diet? (b) Does consumption of fructose induce dyslipidemia compared with consumption of glucose? (c) Is fructose-induced hypertriglyceridemia the result of increased rates

Sickeningly Sweet: Does Sugar Cause Type 2 Diabetes? Yes

“…Baseline glucose levels reduced by 5 mg/dL, glucose area under the curve dropped by 8%, fasting insulin dropped by 10 mU/L, insulin area under the curve dropped 25%-all improved-on the same number of calories and without weight loss, just by removing the added sugar-and in just 10 days! This study alone does not prove that sugar causes metabolic syndrome, but when taken with other studies (2,26,27), Koch postulates for causation were fulfilled.…”

Sex hormone-binding globulin gene expression in the liver: Drugs and the metabolic syndrome

“…The recent study by Stanhope et al (2009) showing that consumption of fructose-sweetened but not glucosesweetened beverages for 10 weeks increases de novo lipid synthesis and impairs insulin sensitivity in overweight or obese adults, implicates fructose as a key nutrient that may contribute to the epidemic of metabolic disorders. The molecular links between SHBG with the risk for Page 15 of 24 A c c e p t e d M a n u s c r i p t 15 developing metabolic disorder associated diseases including hip fracture (Lee et al 2008), breast cancer (Davidson et al 1981;Key et al 1982), and coronary heart disease (Reinecke et al 2002) needs to be investigated further.…”

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