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Published in: Diabetologia 9/2015

01-09-2015 | Review

Fructose and uric acid in diabetic nephropathy

Authors: Petter Bjornstad, Miguel A. Lanaspa, Takuji Ishimoto, Tomoki Kosugi, Shinji Kume, Diana Jalal, David M. Maahs, Janet K. Snell-Bergeon, Richard J. Johnson, Takahiko Nakagawa

Published in: Diabetologia | Issue 9/2015

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Abstract

Clinical studies have reported associations between serum uric acid levels and the development of diabetic nephropathy, but the underlying mechanisms remain elusive. There is evidence from animal studies that blocking uric acid production protects the kidney from tubulointerstitial injury, which may suggest a causal role for uric acid in the development of diabetic tubular injury. In turn, when fructose, which is endogenously produced in diabetes via the polyol pathway, is metabolised, uric acid is generated from a side-chain reaction driven by ATP depletion and purine nucleotide turnover. For this reason, uric acid derived from endogenous fructose could cause tubulointerstitial injury in diabetes. Accordingly, our research group recently demonstrated that blocking fructose metabolism in a diabetic mouse model mitigated the development of tubulointerstitial injury by lowering tubular uric acid production. In this review we discuss the relationship between uric acid and fructose as a novel mechanism for the development of diabetic tubular injury.
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Metadata
Title
Fructose and uric acid in diabetic nephropathy
Authors
Petter Bjornstad
Miguel A. Lanaspa
Takuji Ishimoto
Tomoki Kosugi
Shinji Kume
Diana Jalal
David M. Maahs
Janet K. Snell-Bergeon
Richard J. Johnson
Takahiko Nakagawa
Publication date
01-09-2015
Publisher
Springer Berlin Heidelberg
Published in
Diabetologia / Issue 9/2015
Print ISSN: 0012-186X
Electronic ISSN: 1432-0428
DOI
https://doi.org/10.1007/s00125-015-3650-4

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