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Effect of alloxan diabetes on kidney growth in intact and castrated mice
Abstract:
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.
Insights
Androgen withdrawal reduces mouse kidney weight and RNA synthesis. However, diabetes induction in castrated mice restores kidney weight, indicating renal growth is independent of androgens.
Area of Science:
- Endocrinology
- Renal physiology
Background:
- Mouse kidneys are sensitive to androgen levels.
- Castration (androgen absence) decreases kidney weight and RNA synthesis.
- Alloxan-induced diabetes impacts kidney weight and RNA.
Purpose of the Study:
- To investigate the interplay between androgens and diabetes in regulating mouse kidney weight.
- To determine if androgens are necessary for diabetes-induced renal growth.
Main Methods:
- Surgical castration of mice.
- Induction of diabetes using alloxan injection.
- Measurement of kidney weight and RNA content.
Main Results:
- Castration decreased kidney weight and RNA synthesis.
- Diabetes induction in castrated mice restored kidney weight.
- Diabetes in intact mice increased kidney weight and RNA proportionally.
- Combined castration and diabetes resulted in kidney weight exceeding that of intact animals.
- Renal hypertrophy was the primary driver of renal growth in diabetic mice.
Conclusions:
- Alloxan-induced diabetes promotes renal growth (renotropic effect) independently of androgens.
- Castration does not abolish the renotropic effect of alloxan diabetes in mice.
- Androgens are not required for diabetes-induced renal growth in mice.