Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26049401.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Diabetologia 2015 ; 58 (9): 1993-2002 Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Fructose and uric acid in diabetic nephropathy #MMPMID26049401
Bjornstad P; Lanaspa MA; Ishimoto T; Kosugi T; Kume S; Jalal D; Maahs DM; Snell-Bergeon JK; Johnson RJ; Nakagawa T
Diabetologia 2015[Sep]; 58 (9): 1993-2002 PMID26049401show ga
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.