Abstract
SHBG concentrations in GHD and non GHD children of both sexes were studied in relation to their weight and androgen status. SHBG was inversely related to age in short and control children, but not for GHD. Correction for body weight restored the inverse relationship in these children and improved the correlation for the other groups. DHAS concentrations were similar in GHD and short children, suggesting GH per se does not influence adrenal androgen synthesis. The mean free testosterone in GHD children 12.7 pmol/L, was similar to that in short children, 14.3 pmol/L, and lower than controls 21.2 pmol/L, but consistent with their pubertal status.
The Linear regression of SHBG on IGF-1 was r = -0.605 (P <0.01). It was postulated that IGF-1 and free testosterone may regulate SHBG synthesis.
Administration of native and synthetic GH to prepubertal GHD children lowered SHBG without a significant change in TBG, albumin or free testosterone.
The fall in SHBG concentration after HGH in GHD children is suggested as a selective mechanism which may lead to improved pubertal development.
It is now recognised that many of the biochemical actions of administered human growth hormone (HGH), notably linear growth, protein synthesis and turnover, recorded in the classical studies of Prader et al. (1964), Hubble (1966) and Brown et al. (1967) are mediated by the generation of somatomedin C (IGF-1) (Van Wyk et al., 1974). Less certain is the role that IGF-1 may play in the timing of the growth spurt and subsequent pubertal development. It is documented however, (Laron and Sarel, 1970), that clinical signs of poor genital development in male patients with growth hormone deficiency may be reversed by HGH therapy, but the mechanism is unknown.
A specific carbohydrate rich dimeric binding protein, sex hormone binding globulin, with a high Ka for testosterone and oestradiol-17β is present in serum (Anderson, 1974). Levels are raised prepubertally and fall progressively in both sexes as puberty advances (Lee et al., 1985).
This fall is a trigger for increased levels of free testosterone and oestradiol-17β which may play a part in the activation of the hypothalamic-pituitary-gonadal axis. Preliminary reports (Rudd et al., 1985), have shown that some GHD children had raised SHBG values for chronological and bone age.
These observations suggested that concentrations of non-protein bound sex steroids may be inappropriately low because of a raised In this paper, the weight and the androgen status of GHD SHBG. children is studied in relation to compared to similar data for short addition, the effect of native and Sweden) GH on SHBG and non-protein GHD patients, is examined. their SHBG concentrations and is children and controls. In synthetic (Somatonorm S - Kabi, bound testosterone in the serum of
The relationships of sex hormone‐binding globulin, total testosterone, androstenedione and free testosterone with metabolic and reproductive features of polycystic ovary syndrome