Journal article
Fructose and uric acid in diabetic nephropathy
Diabetologia, Vol.58(9), pp.1993-2002
09/2015
DOI: 10.1007/s00125-015-3650-4
PMCID: PMC4826347
PMID: 26049401
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.
Details
- Title: Subtitle
- Fructose and uric acid in diabetic nephropathy
- Creators
- Petter Bjornstad - Barbara Davis Center for Diabetes, University of Colorado Denver, Aurora, CO, USAMiguel A LanaspaTakuji IshimotoTomoki KosugiShinji KumeDiana JalalDavid M MaahsJanet K Snell-BergeonRichard J JohnsonTakahiko Nakagawa
- Resource Type
- Journal article
- Publication Details
- Diabetologia, Vol.58(9), pp.1993-2002
- DOI
- 10.1007/s00125-015-3650-4
- PMID
- 26049401
- PMCID
- PMC4826347
- ISSN
- 0012-186X
- eISSN
- 1432-0428
- Grant note
- K01 DK095930 / NIDDK NIH HHS R03 DK105041 / NIDDK NIH HHS
- Language
- English
- Date published
- 09/2015
- Academic Unit
- Nephrology; Internal Medicine
- Record Identifier
- 9984094488802771
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