title: Regular moderate exercise reduces advanced glycation and ameliorates early diabetic nephropathy in obese Zucker rats.
abstract: Advanced glycation end products (AGEs) play a key role in the pathogenesis of diabetes and its complications, including the diabetic nephropathy. The renoprotective effects of exercise are well known; however, the mechanisms remain elusive. Here we examined whether a regular moderate exercise in obese Zucker rats (OZR), a model of diabetes- and obesity-associated nephropathy, will affect the development of early renal injury in OZR possibly via alteration of AGEs formation. The OZR were left without exercise (sedentary) or subjected to 10 weeks intermittent treadmill running of moderate intensity. Compared with sedentary OZR, kidneys of running OZR had significantly less glomerular mesangial expansion and tubulointerstitial fibrosis. Running OZR had significantly lower plasma AGEs-associated fluorescence and N(epsilon)-carboxymethyllysine. Correspondingly, renal AGEs and N(epsilon)-carboxymethyllysine content were lower in running OZR. Systemically, exercise increased aerobic metabolism, as apparent from urinary metabolite profiling. No differences in plasma glucose, insulin, or lipid profile were found between the 2 groups. Apart from lower advanced oxidation protein products (a marker of myeloperoxidase activity), no other marker of inflammation was altered by exercise, either systemically or locally in kidneys. No indication of changed oxidative status was revealed between the groups. Exercise in OZR decreased advanced glycation. This might represent the early event of exercise-induced renoprotection in diabetic nephropathy in OZR. If confirmed in clinical studies, regular moderate exercise could represent an easy and effective nonpharmacologic approach to reduce advanced glycation.
authors.affiliation: Department of Clinical and Experimental Pharmacotherapy, Slovak Medical University, 833 03 Bratislava, Slovakia. boor@email.cz
authors.forename: Peter
authors.initials: P
authors.lastname: Boor
authors.forename: Peter
authors.initials: P
authors.lastname: Celec
authors.forename: Michal
authors.initials: M
authors.lastname: Behuliak
authors.forename: Peter
authors.initials: P
authors.lastname: Grancic
authors.forename: Anton
authors.initials: A
authors.lastname: Kebis
authors.forename: Marián
authors.initials: M
authors.lastname: Kukan
authors.forename: Nadezda
authors.initials: N
authors.lastname: Pronayová
authors.forename: Tibor
authors.initials: T
authors.lastname: Liptaj
authors.forename: Tammo
authors.initials: T
authors.lastname: Ostendorf
authors.forename: Katarína
authors.initials: K
authors.lastname: Sebeková
mesh_terms: D000818:Animals; D001835:Body Weight / Q000502:physiology; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism; D003928:Diabetic Nephropathies / Q000378:metabolism* / Q000473:pathology; D005355:Fibrosis; D005920:Glomerular Mesangium / Q000378:metabolism / Q000473:pathology; D017127:Glycation End Products, Advanced / Q000378:metabolism*; D007150:Immunohistochemistry; D007249:Inflammation / Q000473:pathology; D007668:Kidney / Q000473:pathology; D007678:Kidney Glomerulus / Q000378:metabolism / Q000473:pathology; D007684:Kidney Tubules / Q000378:metabolism / Q000473:pathology; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D009765:Obesity / Q000378:metabolism; D009929:Organ Size / Q000502:physiology; D010503:Periodic Acid-Schiff Reaction; D010805:Physical Conditioning, Animal / Q000502:physiology*; D012313:RNA / Q000096:biosynthesis / Q000302:isolation & purification; D051381:Rats; D011924:Rats, Zucker
chemical_list: D017127:Glycation End Products, Advanced; D012313:RNA