title: Functional alterations in the rat kidney induced either by diabetes or high protein diet.
abstract: The aim of this study was to compare the effect of long-term diabetes with that of a long-term high protein diet in vivo on the kidney function and in vitro on cellular parameters of isolated glomeruli of BB rats. Four groups of rats were investigated: Group 1 = normoglycaemic (N) rats > 250 days old; group 2 = age-matched diabetic (D) rats with a diabetes duration of more than 150 days; group 3 = BB rats which were fed a protein diet of 8% (low protein = LP) and group 4 = rats which received a high protein (HP) diet (32%) for more than 80 weeks. From 24-h-urine samples albumin, urea, creatinine and electrolyte excretion were estimated. At the end of the study the total kidney weight was determined and glomeruli were isolated for in vitro experiments. Hyperglycaemic and HP fed rats were characterised by a significantly increased excretion of albumin, urea and different electrolytes compared to normoglycaemic or LP fed animals. Creatinine excretion was neither affected by hyperglycaemia nor HP diet. HP and D caused a significant increase in total kidney weight when compared to the LP and N group, respectively (N: 1.79 +/- 0.08; D: 2.33 +/- 0.09; LP: 2.26 +/- 0.18; HP: 3.28 +/- 0.46 g; p < 0.05). The increased kidney weight of diabetic and HP rats correlated well with a significant enhanced DNA content of isolated glomeruli (N: 3.41 +/- 0.15; D: 4.45 +/- 0.19; LP: 4.18 +/- 0.35; HP: 6.40 +/- 0.62 micrograms/1000 glomeruli; p < 0.02). In addition, glomeruli obtained from either D or HP fed BB rats incorporated significantly more 3H-thymidine into their DNA indicating an elevated rate of DNA synthesis. The results demonstrate that HP diet caused markedly altered kidney function and induced cellular changes of glomeruli which are interpreted as enhanced proliferative processes. These alterations are comparable to those associated with diabetes mellitus. An unbalanced high protein diet represents a considerable risk factor for the development of functional and structural impairments of the kidney and should absolutely be avoided in patients suffering from diseases which are known to be associated with kidney alterations.
authors.affiliation: Institute of Diabetes Gerhardt Katsch Karlsburg, Germany.
authors.forename: A
authors.initials: A
authors.lastname: Dunger
authors.forename: S
authors.initials: S
authors.lastname: Berg
authors.forename: I
authors.initials: I
authors.lastname: Klöting
authors.forename: S
authors.initials: S
authors.lastname: Schmidt
mesh_terms: D000419:Albuminuria; D000818:Animals; D003404:Creatinine / Q000652:urine; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology*; D003928:Diabetic Nephropathies / Q000503:physiopathology*; D004044:Dietary Proteins / Q000494:pharmacology*; D004573:Electrolytes / Q000652:urine; D006943:Hyperglycemia / Q000503:physiopathology; D007668:Kidney / Q000187:drug effects / Q000502:physiology* / Q000503:physiopathology*; D007678:Kidney Glomerulus / Q000502:physiology / Q000503:physiopathology; D051381:Rats; D011913:Rats, Inbred BB; D014508:Urea / Q000652:urine
chemical_list: D004044:Dietary Proteins; D004573:Electrolytes; D014508:Urea; D003404:Creatinine