DIETARY FRUCTOSE AND URINARY OXALATE EXCRETION

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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. Kidney stone disease is a prevalent medical condition that afflicts 10% of Caucasian males at some point in their lifetime with 80% of these stones being predominately calcium oxalate. The amount of oxalate excreted in urine is an important risk factor for stone formation and is derived about equally from dietary intake and endogenous synthesis. The endogenous synthesis of oxalate results from the metabolism of sugars and amino acids and occurs primarily in the liver. Fructose consumption was recently identified as a risk factor for stone formation. Subjects were divided into quintiles and received between 5.6% and 15.2% of their energy as fructose. Several lines of evidence indicate that fructose metabolism results in greater synthesis of oxalate than from the metabolism of glucose. With isolated rat hepatocytes, Rofe et el reported that at sugar concentrations of 10mM, fructose produced 10 times more oxalate than glucose. We have recently observed in preliminary, unpublished experiments that cultured human hepatocytes synthesize 3 times as much oxalate when growing in media containing fructose compared with media containing glucose.