Effect of alloxan diabetes on kidney growth in intact and castrated mice.
The mouse kidney is particularly responsive to the withdrawal or administration of androgens. The absence of endogenous androgens after castration led to decreased RNA synthesis and subsequent decrease in weight of the kidney. The induction of diabetes in 21 days castrated mice restored kidney weight. In intact mice made diabetic by iv injection of alloxan there was a increase in kidney weight. This increase was accompanied by a proportional increase in RNA. In mice hypertrophy was found to be the major factor in renal growth. When castration and diabetes were combined kidney weight did not fall as in the case of castration only but increased even above the kidney weight of intact animals. There was a parallel rise in RNA content of the kidney. Castration does not inhibit the renotropic activity of alloxan diabetes in mice. Renal growth in alloxan diabetes is quite independent of the presence of androgens.
D000728:Androgens / Q000502:physiology; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D002369:Castration; D004247:DNA / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology*; D006984:Hypertrophy; D007668:Kidney / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D051379:Mice; D009929:Organ Size; D012313:RNA / Q000378:metabolism
D000728:Androgens; D001786:Blood Glucose; D012313:RNA; D004247:DNA