A causal role for uric acid in fructose-induced metabolic syndrome

Takahiko Nakagawa,¹ Hanbo Hu,¹Sergey Zharikov,¹Katherine R. Tuttle,²Robert A. Short,^2,3Olena Glushakova,¹Xiaosen Ouyang,¹Daniel I. Feig,⁴Edward R. Block,¹Jaime Herrera-Acosta,⁵ Jawaharlal M. Patel,¹and Richard J. Johnson¹

¹Division of Nephrology, Hypertension, and Transplantation, University of Florida, Gainesville, Florida; ²Department of Research, The Heart Institute of Spokane, and ³Biostatistics, Washington State University, Spokane, Washington; ⁴Division of Nephrology-Medicine, Baylor College of Medicine, Houston, Texas; and ⁵Departamento de Nefrologia, Instituto Nacional de Cardiologia Ignacio Chavez, Tlalpan, Mexico

Am J Physiol Renal Physiol 290: F625-F631, 2006. First published October 18, 2005

American Journal of Renal Physiology

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Amino acids injure mesangial cells by advanced glycation end products, oxidative stress, and protein kinase C

KATHERINE R TUTTLE, EMILY C JOHNSON, SHERYL K COONEY, ROBERT J ANDERBERG, EDWARD K JOHNSON, G DENNIS CLIFTON and RICK L MEEK

The Heart Institute of Spokane and Sacred Heart Medical Center, Spokane, Washington; and Washington State University, Spokane and Pullman, Washington

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Diabetic Kidney Disease: A review of the science. Diabetic Microvascular Complications Today 2:34-37, 2005.

Tuttle, KR.

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Nakagawa T, Tuttle KR, Short RA, Johnson RJ. Hypothesis: fructose-induced hyperuricemia as a causal mechanism for the epidemic of the metabolic syndrome. Nature Clinical Practice Nephrology 1:80-86, 2005.

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Linking Meatabloism and Immunology: Diabetic Nephropathy Is an Inflammatory Disease

Katehrine R. Tuttle, MD

J Am Soc Nephrol 16: 1537-1538, 2005
2005 American Society of Nephrology
doi: 10.1681/ASN.2005040393

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