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Compensatory renal hypertrophy in the absence of androgen binding
Abstract:
As a direct test for a role of androgens, compensatory renal hypertrophy was studied in normal male mice, in androgen-insensitive Tfm/Y mice, and in sibling normal female mice. Fifteen days after unilateral nephrectomy, although the kidneys of the normal male mice were larger, relative increases in renal weight were similar in all groups (33-43%). The magnitude of the increase and the contents of protein, RNA, and DNA were the same in the Tfm/Y mice and the female mice. Androgens are not essential to compensatory renal hypertrophy, but they promote larger mice with larger kidneys.
Insights
Androgens do not drive compensatory renal hypertrophy after kidney removal. However, androgens do contribute to larger body and kidney sizes in male mice.
Area of Science:
- Nephrology
- Endocrinology
- Physiology
Background:
- Compensatory renal hypertrophy (CRH) is the kidney's adaptive response to reduced renal mass.
- The role of androgens in CRH is not fully understood.
Purpose of the Study:
- To investigate the direct role of androgens in compensatory renal hypertrophy.
- To compare CRH in androgen-insensitive mice with normal male and female mice.
Main Methods:
- Unilateral nephrectomy was performed on normal male, androgen-insensitive Tfm/Y, and normal female mice.
- Renal weight, protein, RNA, and DNA content were measured 15 days post-surgery.
Main Results:
- Relative renal weight increase was similar (33-43%) across all groups.
- Tfm/Y mice and female mice showed comparable increases in renal weight and cellular content.
- Normal male mice had larger kidneys, but the relative hypertrophy was not greater.
Conclusions:
- Androgens are not essential for the process of compensatory renal hypertrophy.
- Androgens promote increased overall body and kidney size, independent of the hypertrophic response.