Effect of oral zinc supplements on diaper rash in normal infants.

A total of 89 normal newborn infants received 10mg oral zinc supplements daily for 4 months and 90 others received a placebo. The zinc supplemented group had a significant reduction in the incidence of diaper rash, and they gained slightly more in height and weight, although the growth differences were not significant.

Hair zinc, scalp hair quantity, and diaper rash in normal infants.

Hair zinc concentration was determined by atomic absorption spectrophotometry in 308 normal newborn infants and 199 normal infants aged one to twelve months. Hair zinc concentration declined from 204 micrograms/gm at birth to 112 micrograms/gm at age eight months, and then rose to 144 micrograms/gm at age twelve months. Diaper rash was significantly associated with reduced hair zinc, and infants with the least hair had lower zinc levels than infants with the most hair. The data indicate that hair loss and diaper rash found in normal infants is significantly associated with a reduction in hair zinc concentration.

The effect of sodium selenite toxicity on tissue distribution of zinc, iron, and copper in rats.

Male Sprague-Dawley rats were used to determine the effects of suptoxic and toxic concentrations of selenite in the drinking water on tissue distribution of zinc (Zn), iron (Fe), and copper (Cu). Se (as sodium selenite) was provided in drinking water at concentrations of 0, 2, 4, and 8 ppm. At 19 d, half of the rats in 4 and 8 ppm Sesupplemented groups were kept on drinking water alone for additional 13 d. All rats were sacrificed at the end of 32 d of experiment. Heart, liver, and kidney were analyzed for the concentrations of Fe, Zn, and Cu by atomic absorption spectrophotometry and of Se by a fluorometric method.Results indicated that rats receiving 4 and 8 ppm Se in drinking water showed a marked reduction in food intake and a reduced growth rate. These adverse effects were quickly reversed when high Se intake was discontinued. Se toxicity caused minimal change in zinc status, reduced tissue iron concentrations and caused a marked increase in copper contents in heart, liver, and kidney. The latter findings were only partly reversed after removal of Se in drinking water. The accumulation of Cu in the tissues of Se-toxic rats provides the evidence of some interaction between Se and Cu.

The effects of dietary zinc deficiency on voluntary alcohol drinking in rats.

The effects of dietary zinc deficiency on voluntary alcohol drinking in rats were examined in three separate experiments. Zinc-deficient rats showed a significantly greater voluntary alcohol intake as compared with the pair-fed controls. In the first experiment there were 14 male Sprague-Dawley rats with 7 controls and 7 who were begun on a zinc-deficient diet (below 2 ppm) at body weight 58-81 g. In the second experiment with 11 male Sprague-Dawley rats, the same diet was begun at 103-107 g. In the last experiment, 11 rats were begun at 120-199 g. Hair zinc measurements documented lower levels in the zinc-deficient rats after 6 weeks on the diet. The data indicate that a zinc-deficient state did increase voluntary alcohol intake in rats. In each experiment, the per cent alcohol consumed declined when a normal diet was given after the 6th week, and the difference was significant in experiments 1 and 3.

Growth hormone inhibition causes increased selenium levels in Duchenne muscular dystrophy: a possible new approach to therapy.

Nine children with Duchenne muscular dystrophy were given Sanorex (mazindol), a growth hormone inhibitor, daily for 6 months. There was no significant change in their muscle function, but there was a significant reduction in weight gain and in levels of growth hormone, somatomedin C, hair zinc, serum zinc, and serum LDH. Selenium and glutathione peroxidase in the serum increased significantly. Thirteen other children with growth hormone deficiency had a significant reduction in hair selenium following growth hormone administration. These results show a significant relationship between growth hormone and selenium nutritional status and confirm our previous reports indicating an effect of growth hormone on zinc nutritional status. It is possible that prolonged therapy with a growth hormone inhibitor would attenuate the course and improve the longevity of patients with muscular dystrophy.

Endocrine abnormalities in a patient with partial trisomy 4q.

Partial trisomy of the long arm of chromosome 4, usually resulting from a familial segregation of a balanced translocation, has been described in a number of patients. This report describes the genetic and endocrine findings in a 16 year old 46,XY,12q+ mentally retarded male. The banding pattern of the extra chromatin material from this de novo unbalanced translocation shows that the distal segment of the long arm of chromosome 4 is involved. Comparison of the clinical features in this patient with cases of partial trisomy 4q previously reported support the cytogenetic evidence for this translocation involving the distal portion of 4q. Endocrine data suggested an end-organ resistance, characterised by extreme hyperinsulinaemia, primary hypothyroidism, and hypergonadotrophic hypogonadism associated with no signs of autoimmunity. To our knowledge, no endocrine evaluation has been previously reported in patients with partial trisomy 4q.

Septo-optic dysplasia and median cleft face syndrome in a patient with isolated growth hormone deficiency and hyperprolactinemia.

A pituitary evaluation was carried out in a 12-year-old girl who had early puberty, short stature, optic nerve hypoplasia, and agenesis of the corpus callosum. Her growth hormone (GH) response to insulin-induced hypoglycemia and arginine infusion was blunted. Basal and stimulated levels of prolactin were elevated. The association of GH deficiency and hyperprolactinemia suggests a disruption of the dopaminergic modulation of these hormones. The facial features seen in our patient, such as hypertelorism, V-shaped frontal hairline, and cleft nose and upper lip, are enough to justify the diagnosis of median cleft face (MCF) syndrome. However, the optic nerve hypoplasia and the GH deficiency are characteristics of septo-optic dysplasia, and, to our knowledge, they have never been described in patients with MCF syndrome. Our case fulfills the diagnostic criteria of both, representing a link between both ends of this spectrum.

Synergistic effects of growth hormone therapy on plasma levels of 11-deoxycortisol and cortisol in growth hormone-deficient children.

We have studied the response of blood levels of progesterone, 17-hydroxyprogesterone, 11-deoxycortisol, and cortisol to acute ACTH stimulation in children with isolated GH deficiency. Patients with isolated GH deficiency had generally higher levels of 11-deoxycortisol and lower levels of cortisol than controls both before and after ACTH stimulation. The steroid levels were almost completely restored to control levels after 3 months of treatment with GH. The pre-ACTH treatment levels of 11-deoxycortisol and cortisol were low in patients with both GH and ACTH deficiencies before and during GH therapy. Therefore, GH alone did not appear to have any effect on the hydroxylation of 11-deoxycortisol to cortisol. Before GH therapy, ACTH increased the concentrations of the two steroids. After GH therapy was started, the increase in 11-deoxycortisol was much smaller, but the increase in cortisol was much larger than before therapy. These results suggest a synergistic effect of GH on ACTH action on the biosynthesis of cortisol in the adrenals. Variations in the levels of 11-deoxycortisol and cortisol during hormonal manipulations lead to the identification of the mitochondrial hydroxylation of 11-deoxycortisol as one of the possible sites of action of GH.

Growth hormone receptors in lymphocytes of growth hormone-deficient children.

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.

Effect of oral zinc supplements on growth, hormonal levels, and zinc in healthy short children.

13 short children aged 7-13 years who had a retarded bone age and low hair zinc concentration (under 140 micrograms/g) were treated with oral zinc supplements for a year. There was a significant increase in the growth rate in the children whose hair zinc concentration increased. Growth hormone, testosterone and somatomedin C also increased after oral zinc supplementation. Data from 755 short healthy children who have attended our Growth Clinic are presented which describe their hair and serum zinc concentration at different ages. The data indicate a decline in hair zinc concentration after birth with a gradual increase at age 4-6 years, finally reaching adult normal levels after adolescence.

Manganese in infant formulas and learning disability.

The concentration of manganese in the hair of normal newborn infants was found to increase significantly from 0.19 micrograms/g at birth to 0.965 micrograms/g at 6 weeks of age and 0.685 micrograms/g at 4 months when they were fed infant formula. There was an insignificant increase to 0.330 micrograms/g at age 4 months in breast-fed infants. After this age there was a slow decline in hair manganese to 0.268 micrograms/g in normal children at age 8 years and 0.434 in learning disabled (hyperactive) children. This is the third study reporting elevated hair manganese in learning disabled children.

Effect of growth hormone on hair, serum, and urine zinc in growth hormone-deficient children.

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.

Effects of zinc deficiency and castration on fatty acid composition and desaturation in rats.

The effects of zinc deficiency and testosterone on fatty acid composition of plasma lipids and microsomes of liver, intestine and testes were studied. The activities of fatty acid desaturase (delta 6 and delta 5) in rat liver and testes were also measured. A significant decrease in the level of arachidonic acid was observed in plasma of normal rats fed the zinc-deficient diet. Castration significantly decreased arachidonic acid but increased 20:3 fatty acid, which is negligible in normal rats. Testosterone and zinc administration restored arachidonic acid to normal values. Zinc deficiency does not significantly change the fatty acid profile in liver, but castration decreased both arachidonic and 22:6 fatty acid. Intestinal mucosal microsomes showed that the predominant fatty acid in this tissue, palmitic acid, is independent of zinc status, whereas polyunsaturated fatty acids 18:2 and 20:4 were decreased by zinc-deficient diet or castration. Zinc deficiency sharply decreased 22:5 fatty acid and to some extent, other polyunsaturated fatty acids in testis microsomes. These changes in fatty acids are in agreement with increased delta 9 desaturation and decreased delta 5 desaturase activity. In testes, both delta 6 and delta 5 desaturase activities are decreased in zinc deficiency. It appears that zinc influences the conversion of linoleic to arachidonic acid, whereas testosterone influences delta 6 desaturase activity. The data suggest that zinc deficiency may be one of the important factors in the causation of polyunsaturated fatty acid deficiency, which, in turn, may induce serum hypertriglyceridemia.

Fluorometry of selenium in human hair, urine and blood. A single-tube process for submicrogram determination of selenium.

This communication introduces a special lyophilization process for selenium determination by fluorometric methods. It permits a small sample volume, with several modifications including a single test tube process. Samples and standard are lyophilized first, then digested with nitric-perchloric acid mixture in a heated sand bath. Selenium is complexed with 2,3-diaminonaphthalene and extracted by n-hexane in the same test tube. The n-hexane layer is transferred to a cuvette and measured fluorometrically. Selenium concentration in healthy children from Long Island (aged 5-18 years) was: hair 0.765 +/- 0.114 microgram/g (n = 52), urine 28.65 +/- 8.27 micrograms/g creatinine (n = 66), and serum 95.4 +/- 14.4 ng/ml (n = 44). The current literature reflects an increase in the role of selenium in human nutrition. Thus, a simple but reliable method for determination of selenium in biological materials is needed in the clinical and research laboratory.

Zinc deficiency: improvement in growth and growth hormone levels with oral zinc therapy.

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.

Influence of growth hormone and thyroxine on thermotropic effects of respiration and 1-anilino-8-naphthalene sulfonate fluorescence and on lipid composition of cardiac membranes.

The effects of hypophysectomy and subsequent administration of growth hormone and/or L-thyroxine on thermotropic properties of State 3 respiration (ADP-induced), cholesterol, phospholipid and fatty acid composition of phospholipid fraction were examined in myocardial mitochondria of rats. Temperature-dependence of 1-anilino-8-naphthalene sulfonate fluorescence was determined in vesicles prepared from lipids of heart mitochondria. Transition temperature obtained from the Arrhenius plots of respiration occurred at 21 and 24 degrees C for heart mitochondria of normal and hypophysectomized rats, respectively. Most notably, after hypophysectomy the rate of respiration was lower below 24 degrees C, but was progressively higher above that temperature when compared to normal rats. The energy of activation was 148 and 36% larger below and above the transition temperature, respectively. Growth hormone restored almost completely the energy of activation and respiratory rates to normal levels. Administration of L-thyroxine, with or without growth hormone, did not significantly change the rate of respiration but decreased the transition temperature to 17.7-17.9 degrees C. Lipid and phospholipid content, as well as percent distribution of phospholipids and their fatty acid composition were not statistically different among the different groups of rats. Only cholesterol content was increased after hypophysectomy. Administration of growth hormone and thyroxine did not significantly change the total unsaturation index of fatty acids, but growth hormone increased the content of arachidonic acid (20 : 4) by 70% but decreased the docosahexaenoic acid (22 : 6) three times which may have a beneficial effect on mitochondrial membranes. These and other results suggest that hormones exert different effects on subcellular organelles in different tissues, like heart and liver.