Alteration of urinary sorbitol excretion in WBN-kob diabetic rats - treatment with an aldose reductase inhibitor

in Journal of Endocrinology
Authors:
T Tsugawa
Search for other papers by T Tsugawa in
Current site
Google Scholar
PubMed
Close
,
R Shinohara
Search for other papers by R Shinohara in
Current site
Google Scholar
PubMed
Close
,
A Nagasaka
Search for other papers by A Nagasaka in
Current site
Google Scholar
PubMed
Close
,
I Nakano
Search for other papers by I Nakano in
Current site
Google Scholar
PubMed
Close
,
F Takeda
Search for other papers by F Takeda in
Current site
Google Scholar
PubMed
Close
,
M Nagata
Search for other papers by M Nagata in
Current site
Google Scholar
PubMed
Close
,
N Oda
Search for other papers by N Oda in
Current site
Google Scholar
PubMed
Close
,
Y Sawai
Search for other papers by Y Sawai in
Current site
Google Scholar
PubMed
Close
,
N Hayakawa
Search for other papers by N Hayakawa in
Current site
Google Scholar
PubMed
Close
,
A Suzuki
Search for other papers by A Suzuki in
Current site
Google Scholar
PubMed
Close
, and
M Itoh
Search for other papers by M Itoh in
Current site
Google Scholar
PubMed
Close
Free access

Sign up for journal news

An accelerated polyol pathway in diabetes contributes to the development of diabetic complications. To elucidate diabetic nephropathy involving also renal tubular damage, we measured urinary sorbitol concentration concomitantly with urinary N-acetyl-D-glucosaminidase (NAG) excretion in WBN-kob diabetic rats.Twenty-four-hour urinary sorbitol concentrations increased in the diabetic rats in parallel with whole blood sorbitol concentrations. An increase in 24-h urinary NAG excretion coincided with the elevated urinary sorbitol levels in the diabetic rats. The administration of epalrestat, an aldose reductase inhibitor, reduced the increased whole blood and urinary sorbitol concentrations and urinary NAG excretion concomitantly with renal aldose reductase inhibition in the diabetic rats.These results indicate that diabetic nephropathy involves distorted cell function of renal tubules, and that treatment with epalrestat may prevent at least the progress of the nephropathy.