madman
Super Moderator
The effects of growth hormone (GH) on sodium retention and extracellular fluid (ECF) are well established. The mechanisms are not clear but are thought to involve the GH/IGF-I (insulin-like growth factor I) axis. Men and women differ in their ECF and this contributes to men’s higher fat-free mass. Johannsson et al. investigated the effects of testosterone in natriuresis and showed that this hormone significantly increases ECF, an effect that is augmented by GH.
Testosterone normally stimulates GH secretion, so this study examined men who had GH deficiency and hypogonadotrophic hypogonadism. In the first study group, 10 subjects were given GH, alone or with testosterone, in a protocol that allowed the effects of GH to be compared with GH plus testosterone. Serum IGF-I levels and ECF increased significantly in response to GH; testosterone showed additive effects, but these were not statistically significant.
In the complementary protocol, nine subjects were given testosterone, alone or with GH, such that the effects of testosterone could be compared with testosterone plus GH. Testosterone had no effect on IGF-I levels but the addition of GH significantly increased these levels. However, testosterone did significantly increase ECF, an effect that was also significantly enhanced by the addition of GH.
The mechanisms of testosterone’s effects are not known but it could act directly on renal tubules to increase fluid retention. These novel findings of testosterone’s role in ECF suggest that it may play a part in the observed gender differences in fat-free mass and responses to GH replacement therapy.
Testosterone normally stimulates GH secretion, so this study examined men who had GH deficiency and hypogonadotrophic hypogonadism. In the first study group, 10 subjects were given GH, alone or with testosterone, in a protocol that allowed the effects of GH to be compared with GH plus testosterone. Serum IGF-I levels and ECF increased significantly in response to GH; testosterone showed additive effects, but these were not statistically significant.
In the complementary protocol, nine subjects were given testosterone, alone or with GH, such that the effects of testosterone could be compared with testosterone plus GH. Testosterone had no effect on IGF-I levels but the addition of GH significantly increased these levels. However, testosterone did significantly increase ECF, an effect that was also significantly enhanced by the addition of GH.
The mechanisms of testosterone’s effects are not known but it could act directly on renal tubules to increase fluid retention. These novel findings of testosterone’s role in ECF suggest that it may play a part in the observed gender differences in fat-free mass and responses to GH replacement therapy.
