Effects of inhibition of glycation and oxidative stress on the development of diabetic nephropathy in rats.
(2002) In Journal of Diabetes and its Complications 16(6). p.395-400- Abstract
- We investigated whether aminoguanidine (AG), an inhibitor of advanced glycated end product formation, or probucol (PB), a free radical scavenger, could influence signs of glomerular and distal tubular function and morphological changes in kidneys of male Wistar rats after 6 months of streptozocin (STZ)-induced diabetes. Diabetic rats had a higher kidney weight/body weight ratio (P<.001), but neither AG nor PB influenced the increased ratio. Diabetes caused an increased urinary albumin excretion (P<.05), which was normalized by AG, but further exaggerated by PB (P<.001). Diabetes also caused an increase in the urinary excretion of Tamm–Horsfall protein (P<.001). Both AG and PB attenuated this increase (P<.05 for both). A few... (More)
- We investigated whether aminoguanidine (AG), an inhibitor of advanced glycated end product formation, or probucol (PB), a free radical scavenger, could influence signs of glomerular and distal tubular function and morphological changes in kidneys of male Wistar rats after 6 months of streptozocin (STZ)-induced diabetes. Diabetic rats had a higher kidney weight/body weight ratio (P<.001), but neither AG nor PB influenced the increased ratio. Diabetes caused an increased urinary albumin excretion (P<.05), which was normalized by AG, but further exaggerated by PB (P<.001). Diabetes also caused an increase in the urinary excretion of Tamm–Horsfall protein (P<.001). Both AG and PB attenuated this increase (P<.05 for both). A few glomeruli displayed focal thickening of varying degrees. Silver staining disclosed the glomerulopathy to be intercapillary glomerulosclerosis. Rats on PB-enriched diet displayed less pronounced changes than untreated rats (P<.01), while AG had no effect. The results suggest that oxidative stress could be involved in the development of diabetic nephropathy. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/114635
- author
- Agardh, Carl David ; Stenram, Unne LU ; Torffvit, Ole LU and Agardh, Elisabet LU
- organization
- publishing date
- 2002
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Free Radical Scavengers: pharmacology, Diabetic Nephropathies: physiopathology, Disease Progression, Experimental: physiopathology, Probucol: pharmacology, Rats, Animal, Diabetes Mellitus, Non-U.S. Gov't, Distal: physiopathology, Male, Oxidative Stress: physiology, Support, Wistar, Kidney Tubules, Distal: pathology, Distal: drug effects, Kidney Glomerulus: physiopathology, Kidney Glomerulus: pathology, Kidney Glomerulus: drug effects, Guanidines: pharmacology, Advanced: antagonists & inhibitors, Glycosylation End Products, Glycosylation
- in
- Journal of Diabetes and its Complications
- volume
- 16
- issue
- 6
- pages
- 395 - 400
- publisher
- Elsevier
- external identifiers
-
- wos:000179378700006
- scopus:0036860156
- ISSN
- 1873-460X
- DOI
- 10.1016/S1056-8727(02)00164-2
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Medicine (Lund) (013230025), Ophthalmology (013242810), Pathology, (Lund) (013030000), Endocrinology (013241500)
- id
- bb1bd286-a922-4d53-ac69-57e9c4bf82d2 (old id 114635)
- alternative location
- http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12477624&dopt=Abstract
- date added to LUP
- 2016-04-01 15:48:21
- date last changed
- 2024-02-26 07:49:27
@article{bb1bd286-a922-4d53-ac69-57e9c4bf82d2, abstract = {{We investigated whether aminoguanidine (AG), an inhibitor of advanced glycated end product formation, or probucol (PB), a free radical scavenger, could influence signs of glomerular and distal tubular function and morphological changes in kidneys of male Wistar rats after 6 months of streptozocin (STZ)-induced diabetes. Diabetic rats had a higher kidney weight/body weight ratio (P<.001), but neither AG nor PB influenced the increased ratio. Diabetes caused an increased urinary albumin excretion (P<.05), which was normalized by AG, but further exaggerated by PB (P<.001). Diabetes also caused an increase in the urinary excretion of Tamm–Horsfall protein (P<.001). Both AG and PB attenuated this increase (P<.05 for both). A few glomeruli displayed focal thickening of varying degrees. Silver staining disclosed the glomerulopathy to be intercapillary glomerulosclerosis. Rats on PB-enriched diet displayed less pronounced changes than untreated rats (P<.01), while AG had no effect. The results suggest that oxidative stress could be involved in the development of diabetic nephropathy.}}, author = {{Agardh, Carl David and Stenram, Unne and Torffvit, Ole and Agardh, Elisabet}}, issn = {{1873-460X}}, keywords = {{Free Radical Scavengers: pharmacology; Diabetic Nephropathies: physiopathology; Disease Progression; Experimental: physiopathology; Probucol: pharmacology; Rats; Animal; Diabetes Mellitus; Non-U.S. Gov't; Distal: physiopathology; Male; Oxidative Stress: physiology; Support; Wistar; Kidney Tubules; Distal: pathology; Distal: drug effects; Kidney Glomerulus: physiopathology; Kidney Glomerulus: pathology; Kidney Glomerulus: drug effects; Guanidines: pharmacology; Advanced: antagonists & inhibitors; Glycosylation End Products; Glycosylation}}, language = {{eng}}, number = {{6}}, pages = {{395--400}}, publisher = {{Elsevier}}, series = {{Journal of Diabetes and its Complications}}, title = {{Effects of inhibition of glycation and oxidative stress on the development of diabetic nephropathy in rats.}}, url = {{http://dx.doi.org/10.1016/S1056-8727(02)00164-2}}, doi = {{10.1016/S1056-8727(02)00164-2}}, volume = {{16}}, year = {{2002}}, }