This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Fructose consumption has risen sharply during the past several decades. Since its introduction to the United States in 1967, high fructose corn syrup-HFCS has overtaken sucrose as the main sweetener in manufactured foods and beverages, and is responsible for the approximately 30% increase in fructose in our diet. Numerous studies have shown that excessive fructose consumption can cause a variety of harmful metabolic effects, suggesting that fructose may partially be responsible for the current epidemic in obesity, hypertension, metabolic syndrome, and diabetes. There has been some variability in the findings, which could be related to varying responses to fructose among individuals. There is a lack of studies investigating if the source of dietary fructose, sucrose versus high fructose corn syrup, impacts the body differently, influencing the development of various health problems. We propose to conduct a preliminary study to investigate the pharmacokinetics and pharmacodynamics of fructose in a broad population. The goal of our research is to compare the impact of the two main sources of dietary fructose, sucrose versus HFCS, on fructose bioavailability and acute metabolic changes by measuring response phenotypes, such as serum uric acid, lactate, and triglyceride levels. This study will advance our understanding of the differences in the pharmacokinetics and pharmacodynamics of fructose from two main dietary sweeteners: sucrose versus high fructose corn. These findings will allow us to determine if fructose and factors determining its levels can be potential targets for the therapy and prevention of these epidemic health problems.
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