ABSTRACT
Human growth hormone was injected intravenously into 18 growth hormone-deficient children and growth hormone binding sites in lymphocytes were investigated. Fresh circulating lymphocytes had a low initial value for the binding of growth hormone to solubilized receptors (3.45 +/- 1.46%) but after growth hormone injection, the binding rapidly increased to 14.8 +/- 4.2% at 2 1/2 h and 8.7 +/- 1.8% at 5 h. The sharp increase in binding is due to increase in the number of binding sites. Two control children who received chorionic gonadotropin had no change in lymphocyte growth hormone receptors. The methodological differences between the present study and previous attempts to identify human growth receptors in lymphocytes were (1) lymphocytes were separated and disrupted with Triton X-100 as quickly as possible (to avoid error from receptor leaking out of the cell) and (2) the receptors were assayed at 2 1/2 h after growth hormone administration (previous studies were 12-24 h later). One possible explanation for the data is that growth hormone receptor from liver is taken up by lymphocytes and rapidly released again, thus, contributing to the hormonal receptor economy in humans.
Subject(s)
Growth Hormone/deficiency , Lymphocytes/metabolism , Receptors, Cell Surface/metabolism , Adolescent , Child , Child, Preschool , Female , Humans , Male , Receptors, Somatotropin , SolubilityABSTRACT
The present study shows that growth hormone administration to 30 growth hormone-deficient children significantly increased their hair zinc concentration (147.0 +/- 31.9 micrograms/ml before, and 168.7 +/- 30.4 micrograms/g after) and decreased their urinary zinc excretion (514 +/- 170 micrograms/g creatine before and 353 +/- 162 micrograms/g creatinine after), suggesting a role for growth hormone in zinc metabolism in children. Since the increase in hair zinc was similar to that found with testosterone on human growth, we speculate that at least some of the anabolic effects of growth hormone and androgens are mediated through their effect on zinc metabolism.
Subject(s)
Growth Hormone/deficiency , Hair/metabolism , Zinc/metabolism , Adolescent , Child , Female , Growth/drug effects , Growth Hormone/pharmacology , Humans , Male , Zinc/pharmacologyABSTRACT
A 14-year-old girl and a 13-year-old boy were found to be growth hormone deficient by insulin-arginine stimulation tests, and were also found to be zinc deficient. When oral zinc replacement was given, they both had a significant increase in growth rate which continued for at least 2 years, and subsequent growth hormone tests were normal.
Subject(s)
Growth Disorders/drug therapy , Zinc/therapeutic use , Administration, Oral , Adolescent , Female , Growth Hormone/analysis , Humans , Male , Zinc/deficiencyABSTRACT
We describe a premature female infant exposed in utero to danazol during the first trimester of pregnancy. She was first observed in the newborn period with marked degree virilization and clinical findings suggestive of salt-losing congenital adrenal hyperplasia. This was supported by the high plasma levels of 17 alpha-hydroxyprogesterone and adrenocorticotropic hormone and low plasma cortisol level. Levels of testosterone, androstenedione, 11-deoxycortisol, and renin were also elevated. An excessive increase in the levels of 17 alpha-hydroxyprogesterone and 11-deoxycortisol to corticotropin administration associated with impaired increase in plasma cortisol level strongly suggests a partial block in the 21-hydroxylation of 17 alpha-hydroxyprogesterone. However, the high levels of 11-deoxycortisol also suggest a block of the steroid 11 beta-monooxygenase. A year later she was found to have normal basal levels of the adrenal steroids and normal response to corticotropin administration, pointing out the transitory nature of these abnormalities. It may be hypothesized that danazol produced a transitory block of the steroid 21- and 11 beta-monooxygenases in this child.
Subject(s)
Adrenal Hyperplasia, Congenital/chemically induced , Danazol/adverse effects , Infant, Premature, Diseases/chemically induced , Pregnadienes/adverse effects , Adrenal Hyperplasia, Congenital/blood , Adrenocorticotropic Hormone/blood , Androstenedione/blood , Cortodoxone/blood , Cosyntropin , Female , Humans , Hydrocortisone/blood , Hydroxyprogesterones/blood , Infant, Newborn , Maternal-Fetal Exchange , Pregnancy , Pregnancy Trimester, First , Renin/blood , Testosterone/bloodABSTRACT
Zinc levels were measured in hair and serum of boys with constitutional growth delay and familial short status and in several boys before and after oral administration of methyltestosterone. These results show the following: (1) zinc levels in boys beyond stage 3 of genital development are significantly higher than in stage 1 and 2; (2) there is a linear relationship between zinc levels and serum testosterone concentration (up to 250 ng/dL); and (3) methyltestosterone administration raised the zinc concentration in serum and hair, especially in boys with constitutional growth delay. Therefore, increased endogenous production or exogenous supply of testosterone are associated with increased zinc levels. We speculate that the relative testosterone deficiency and hypogonadotropism seen in constitutional growth delay may result in decreased zinc levels, which in turn could cause a further delay in the appearance of secondary sexual characteristics and greater growth retardation.
