The uptake of prolactin into female rat liver. Concentration of intact hormone in the Golgi apparatus.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Z Josefsberg.
Explore the source record for details and available documents.
Two groups of hHG deficient adolescents (isolated growth hormone deficiency: 11 patients and multiple pituitary hormone deficiency: 20 patients) receiving hGH therapy were analyzed for their linear growth response. It was found that even at a chronological age of 15 years or more, growth can be markedly enhanced, depending upon the bone age and pubertal stage in the IGHD patients and upon optimal balance between hGH and sex hormones in the MPHD patients.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Insulin binding to Golgi and plasmalemma fractions from the liver of obese (ob/bo and db/db) and lean control mice was studied. The specficiity of binding in Golgi fractions (Golgi vesicles and Golgi cisternae) was identical to that observed previously in rat liver Golgi fractions and plasmalemma. Binding to plasmalemma was much lower in obese compared to lean mice, but binding to Golgi cisternae was either not changed (ob/ob) or slightly increased (db/db) in obese compared to lean littermates. These observations suggest that intracellular (Golgi cisternae) insulin receptors are regulated differently from those of the plasmalemma. We propose that insulin affects hepatic receptor content in two different ways. On the one hand plasmalemma receptor loss is accelerated, and on the other hand intracellular receptor production is increased. This model can explain in one framework the effect on insulin in reducing and prolactin in augmenting the level of their respective hepatic receptors.
The plasma insulin response to a standard arginine stimulation test was studied in 247 children and adolescents (177 males and 70 females) with constitutional growth retardation as compared with the response obtained in a matched group of 42 normal subjects and a group of 57 obese subjects. When the insulin response was related to pubertal ratings in the children and adolescents with growth retardation, it was found that the mean fasting levels and mean peak response both rose with the progression of puberty. This tendency was more pronounced in the females. When the insulin response was related to the degree of adiposity as measured by the degree of subscapular skinfold thickness, it was found that the greater the adiposity, the greater was the mean response, with the females showing higher levels than the males in each group. Even when the response in the two sexes was compared in subjects of a similar age and skinfold thickness, the females had a higher mean peak insulin response than did the males.
Six children and adolescents (aged from 2 6/12 to 16 years) with isolated hGH deficiency were subjected to a standard oral glucose tolerance test (OGTT) followed by the administration of IV glucagon at 180 mins. Three of them underwent a second test after several months of hGH therapy. Nine patients underwent a separate IV glucagon test and two of these patients had both tests. As controls served 14 endocrinologically normal children and adolescents, who underwent both tests. It was found that the patients with isolated hGH deficiency had lower basal insulin and blood glucose levels and that their insulin response to IV glucagon even after oral glucose preloading was significantly lower than in the control group. This response was partially restored by several months of hGH treatment in the three patients tested. These findings are interpreted as further evidence for an insulinotrophic effect of hGH.
Penile length and circumference were measured in twenty boys with isolated gonadotrophin deficiency, before and during the administration of androgen therapy. Their age ranged between 3 and 20 years. Considering as normal, measurements above the tenth centile, in all the patients but four the penile length was below normal, and in two it was borderline. Penis circumference was normal in two, borderline in four and subnormal in sixteen. Regular administration of androgen therapy increased penile length in eleven out of fourteen patients with achievement of normal length in four. It is concluded that congenital lack of LH and testicular androgen activation causes small sized penises, even in the prepubertal period. Gonadotrophin deficiency should be looked for in patients with measurements below the tenth centile. Early diagnosis and institution of androgen therapy between 11 and 12 years is likely to increase penile size and prevent the psychological side effects of undersized genitals and delayed puberty.
Thirty-seven children and adolescents of several diagnostic entitites (constitutional growth retardation, diabetes mellitus and pituitary insufficiency) were tested with an i.v. bolus injection of glucagon for plasma human growth hormone (HGH) response. Most of the subjects were also tested for the same purpose by the arginine stimulation test, and the data were compared. It was found that i.v. glucagon is a potent stimulus of human growth hormone release. The HGH is released in two peaks, the first one occuring within 30 min, most probably by a direct effect. The second peak occurs after 120 min, most probably as a secondary effect caused by the drop in blood glucose after its initial rise, which is induced by glucagon. The peak concentrations of HGH induced by glucagon, were very similar to those provoked by i.v. arginine in the same subjects.
Fourteen children and adolescents with slight constitutional growth retardation (12 males and two females) aged from 7 1/2 to 18 1/2 yr underwent an oral glucose tolerance test (OGTT 1.75 g/Kg followed at 180 min by an i.v. glucagon injection (0.03 mg/Kg). On a separate occasion these children underwent a simple i.v. glucagon test. Comparing the glucose and insulin response in the two glucagon tests for each child we found that whereas in the single test the blood glucose rose slowly with a peak at 30 min, in the combined test the peak was at 5 min. The mean peak values were similar (129 and 121 mg/100 ml). The mean peak insulin response in the single test was 70 muU/ml (at 2 min) as compared to 253 muU/ml (at 2 min) in the combined test. Our studies provide further evidence for a direct effect of glucagon on insulin release and that glucose preloading augments this effect, without relation to the concomitant blood glucose concentrations.
Two brothers with Reifenstein syndrome underwent LH-RH and HCG tests at various ages ranging from 13 to 17 years. We found that at age 13 the plasma LH and FSH response to one LH-RH injection was normal. After the age of 14, the basal plasma concentration of LH and FSH and their response to LH-RH became elevated. Concomitantly the plasma testosterone levels rose to abnormal levels. These findings are compatible with progressive development of primary gonadal dysfunction and with peripheral insensitivity to testosterone.
Explore the source record for details and available documents.
The plasma and urinary testosterone response to one i.m. injection of 5,000 IU human chorionic gonadotropin (HCG) was tested in 45 children and adolescents of several diagnostic entities: testosterone was measured before the injection and on the second, fourth and sixth days thereafter. It was found that there was a better correlation between the testosterone concentrations and the different pubertal stages than between testosterone concentration and either chronological or skeletal age. In the children with normal pubertal development, there was a slight rise in basal testosterone concentration with the progression of the pubertal stages. HCG caused a rise in plasma and urinary testosterone: this response was more marked in pubertal stages 4 and 5. The urinary response was variable whereas the changes in plasma testosterone concentration were more constant. In children and adolescents with primary or secondary hypogonadism, the basal levels of testosterone were low or undetectable and there was only a slight response to the single dose of HCG. It was concluded that a single i.m. injection of 5,000 IU HCG and the determination of plasma testosterone before, and two and four days after injection is a useful screening test for Leydig cell function.
Sixty-three normal, healthy children and adolescents (39 males and 24 females) ranging in age from 2 to 20 years, were given a standard oral glucose tolerance test. A tendency to higher blood glucose levels and a statistically significant increase in insulin levels were found in the older age group in response to the glucose load. The older age group showed a significantly higher response of both glucose and insulin when separate percentile curves for prepubertal and pubertal boys and girls were constructed. No statistical differences were found between the sexes. Our findings demonstrate the necessity of applying norms for the oral glucose tolerance test according to age, particularly with respect to insulin values. The possibility of additional differences in response among various populations, as apparent from a comparison with the results of several other investigators, requires further study.
Explore the source record for details and available documents.
Plasma glucagon response to an arginine infusion was studied in children and adolescents belonging to the following groups: (I) twenty-two controls; (II) six subjects with delayed insulin peak during oral GTT; (III) ten diabetics on diet and/or oral therapy; (IV) six newly diagnosed uncompensated diabetics; and (V) eight diabetics on insulin therapy. The fasting glucagon concentrations and rise of glucagon in response to arginine in the patients of Groups II, III and V were similar to those of the controls (Group I). The basal levels and rise of glucagon in the newly diagnosed, uncompensated dibetic children (Group IV) was elevated compared to the other groups but the difference was statistically not significant. The results of this investigation favour the hypothesis that the hyperglucagonaemia in diabetes is a secondary effect to the metabolic derangement, bearing a direct relationship to the degree of homeostastic decompensation.
Explore the source record for details and available documents.
Explore the source record for details and available documents.