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There is ample evidence, both in humans and in animal models, that a high sugar intake can cause obesity, dyslipidemia, hepatic and extrahepatic insulin resistance, and hepatic steatosis. These deleterious effects have been shown to be specifically due to the fructose component of sugars. Little is known regarding whether the effects of fructose can be modulated by other environmental factors, however. Here, we hypothesize that the effects of fructose depend tightly on the environment. We specifically hypothesize 1) that exercise protects against the deleterious effects of high fructose intake, 2) that fructose will exert more detrimental effects when it is consumed together with a diet high in carbohydrate from refined carbohydrates, and that a diet rich in unrefined cereals and whole grains will exert a protective effects, and 3) that a moderate fructose intake, which would not produce adverse effects of its own, has deleterious effects when consumed together with another well known hepatotoxin, alcohol. To evaluate these hypotheses, we plan to perform 3 proof-of-concept studies in healthy volunteers. In one of these studies, we will test the short term effects of a high fructose intake with and without exercise on various metabolic markers. In the second study, we will test the short term effects of a high carbohydrate diet from either refined cereals or whole grain on fructose-induced lipid synthesis. In the third study, we will test the acute and short term ( 7 days) effects of fructose alone, alcohol alone, or fructose + alcohol on markers of metabolic disorders and of liver damage. The results of these studies are expected to demonstrate the concept that the adverse effects of fructose can indeed be reduced or enhanced by other environmental factors, and to identify the mechanisms involved in fructose-environment interactions