THE SERUM HALF-LIFE OF SOMATOMEDIN ACTIVITY: EVIDENCE FOR GROWTH HORMONE DEPENDENCE

1976 ◽  
Vol 83 (2) ◽  
pp. 243-258 ◽  
Author(s):  
Kenneth L. Cohen ◽  
S. Peter Nissley
Keyword(s):  
Growth Hormone ◽  
Half Life ◽  
Thymidine Incorporation ◽  
Analysis Data ◽  
Normal Serum ◽  
Rat Serum ◽  
Thymidine Incorporation Assay ◽  
Hypophysectomized Rats ◽  
Normal Rat ◽  
Incorporation Assay

ABSTRACT The serum half-life of somatomedin (SM) activity has been measured following the intravenous injection of SM activity into hypophysectomized rats. A [3H]thymidine incorporation assay in chick embryo fibroblasts (CEFs) has been utilized to measure SM activity. Cell cycle analysis data obtained with the flow microfluorometer shows that the [3H]thymidine incorporation data reflects actual DNA synthesis. When normal rat serum was injected, a half-life for SM activity of approximately 3 h was determined. In marked contrast, when serum from hypophysectomized (hypox) rats acutely treated with growth hormone (GH) was used as the source of SM actively, the half-life of the SM actively was short, approximately 8 min. However, when serum from hypox rats chronically treated with GH was injected, the half-life was again long, approximately 4 h. SM activity has been separated from its binding proteins by boiling under acid conditions or chromatography on Sephadex G-50 in 1 n acetic acid. The halflife of this partially purified SM activity was short, in the range of 10–30 min. Finally, recombination of the partially purified SM activity with the large proteins in normal serum extended the half-life of the SM from 10–30 min to about 2 h. These data indicate that the serum half-life of SM activity is GH dependent and suggest that the serum binding protein, like SM itself, is under GH control.

FUNCTIONAL HETEROGENEITY OF THE THYROID AND POSSIBLE PRESENCE OF IODOTYROSINE-LIKE COMPOUNDS IN NORMAL SERUM

1965 ◽  
Vol 48 (2) ◽  
pp. 199-208 ◽  
Author(s):  
J. D. Wiener
Keyword(s):  
Human Subjects ◽  
Thyroid Tissue ◽  
Normal Serum ◽  
Schematic Model ◽  
Functional Heterogeneity ◽  
Rat Serum ◽  
Iodine Metabolism ◽  
Normal Rat ◽  
Isotope Equilibrium ◽  
Equilibrium Experiment

ABSTRACT After the administration of 131I to normal animals or human subjects, labelled thyroxine and triiodothyronine, but at most traces of labelled iodotyrosines can be detected in the serum. However, several investigators using various methods claim to have found considerable amounts of one or both of these iodotyrosines when assaying the stable (non-radioactive) iodinated compounds in the serum. Considering the available evidence as convincing for the present, an attempt has been made to explain this discrepancy. A schematic model of the thyroidal iodine metabolism is proposed, based on (a) the hypothesis that the iodotyrosines are present in the circulation in a »masked« form (i. e. protected against deiodination), and (b) the known functional heterogeneity of the thyroid tissue. This heterogeneity should be of a qualitative as well as quantitative nature. As the physical decay rate of 131I is short in comparison with the turnover rate of the masked iodotyrosine pool, an isotope equilibrium experiment with rats was carried out, using the long-lived isotope 125I. The results of this experiment, viewed together with those of a similar investigation published by others, seem to lend support to the proposed mechanism. The presence of non-negligible amounts of a diiodotyrosine-like compound in normal rat serum seems fairly well established.

scholarly journals Streptozotocin and Alloxan-based Selection Improves Toxin Resistance of Insulin-Producing RINm Cells

2000 ◽  
Vol 1 (3) ◽  
pp. 211-219 ◽  
Author(s):  
Konstantin O. Bloch ◽  
Romy Zemel ◽  
Olga V. Bloch ◽  
Hagar Grief ◽  
Pnina Vardi
Keyword(s):  
Thymidine Incorporation ◽  
Colorimetric Method ◽  
Hormone Production ◽  
Partial Protection ◽  
Toxin Resistance ◽  
Cell Defense ◽  
Thymidine Incorporation Assay ◽  
Incorporation Assay ◽  
Al Treatment ◽  
Selection Of

The aim of our study was to develop a method for selection of subpopulations of insulin producing RINm cells with higher resistance to beta cell toxins. Cells, resistant to streptozotocin (RINmS) and alloxan (RINmA), were obtained by repeated exposure of parental RINm cells to these two toxins, while the defense capacity, was estimated by the MTT colorimetric method, and[H3]-thymidine incorporation assay. We found that RINmS and RINmA displayed higher resistance to both streptozotocin (STZ) and alloxan (AL) when compared to the parental RINm cells. In contrast, no differences in sensitivity to hydrogen peroxide were found between toxin selected and parental cells. Partial protection from the toxic effect of STZ and AL was obtained only in the parental RINm cells after preincubation of cells with the unmetabolizable 3- O-methyl-glucose. The possibility that GLUT-2 is involved in cell sensitivity to toxins was confirmed by Western blot analysis, which showed higher expression of GLUT-2 in parental RINm compared to RINmS and RINmA cells. In addition to the higher cell defense property evidenced in the selected cells, we also found higher insulin content and insulin secretion in both RINmS and RINmA cells when compared to the parental RINm cells. In conclusion, STZ and AL treatment can be used for selection of cell sub-populations with higher cell defense properties and hormone production. The different GLUT-2 expression in parental and re sistant cells suggest involvement of GLUT-2 in mechanisms of cell response to different toxins.

Effect of chronic administration of insulin on pituitary gland content of growth hormone in the normal rat

1970 ◽  
Vol 48 (2) ◽  
pp. 85-89 ◽  
Author(s):  
Robert L. Hazelwood ◽  
John G. Galaznik
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Young Adult ◽  
Pituitary Gland ◽  
Chronic Administration ◽  
Female Rats ◽  
Pituitary Glands ◽  
Hypophysectomized Rats ◽  
Normal Rat ◽  
Gland Content

Acetone-dried pituitary glands from young adult female rats (starting weight 165–168 g) previously injected (s.c.) with doses of insulin of 0.5 U to 1.0 U/kg body weight for 4 days, and then with 2.0 U/kg 6 days a week for an additional 34 days, were bioassayed in young hypophysectomized rats for growth hormone content. Insulin-injected rats gained significantly more weight than saline-injected controls. The tibia cartilage width of the insulin-injected donor rats was greater than that of control rats after 9, 17, 24, and 31 days of insulin; pituitary gland preparations from these insulin-injected rats increased tibia cartilage widths slightly but significantly over those of rats injected with control pituitary gland preparations.

scholarly journals Extraction of an Erythropoietin-Producing Factor from a Particulate Fraction of Rat Kidney

Blood ◽  
1966 ◽  
Vol 28 (3) ◽  
pp. 330-343 ◽  
Author(s):  
JOSEPH F. CONTRERA ◽  
ALBERT S. GORDON ◽  
ARTHUR H. WEINTRAUB
Keyword(s):  
Rat Kidney ◽  
Deae Cellulose ◽  
Mitochondrial Fraction ◽  
Normal Serum ◽  
The Other ◽  
Step Method ◽  
Renal Vasculature ◽  
Rat Serum ◽  
Normal Rat ◽  
Strong Resemblance

Abstract 1. A two-step method for the extraction of erythropoietin from hypoxic kidneys has been developed which allows residual plasma erythropoietin in renal vasculature to be separated from that of intracellular origin. 2. Renal extracts have been purified by DEAE cellulose chromatography and found to contain 2 major erythropoietically active fractions. One bears strong resemblance to plasma erythropoietin. The other component is unique in that it has practically no erythropoietic-stimulating activity unless previously incubated with normal rat serum. This activation phenomenon is used to identify this kidney component as the renal erythropoietic factor (REF). The REF has the capacity to produce erythropoietin or become erythropoietically active when incubated with normal rat serum. 3. Differential centrifugation technics revealed that the REF is confined to particles present in the light mitochondrial fraction of kidney. 4. Extracts of the light mitochondrial fraction of kidneys from normal rats produced significant amounts of erythropoietin when incubated with normal serum. The quantity found, however, was less than that evoked by similar extracts of kidneys from hypoxic rats. 5. The product of the incubation extracts of the renal light mitochondrial fraction with normal rat serum showed the same log dose/response regression as sheep plasma erythropoietin standard. 6. It is hypothesized that either (a) the REF is a precursor of erythropoietin which must be complexed with a carrier present in normal serum in order to become physiologically active, or (b) the renal factor is an enzyme which produces erythropoietin by its action on a particular serum protein.

Synergistic effects of endothelin-1 (ET-1) and transforming growth factor alpha (TGF-α) or epidermal growth factor (EGF) on DNA replication and G1 to S phase transition

1991 ◽  
Vol 11 (3) ◽  
pp. 171-180 ◽  
Author(s):  
Yun-Chi Yeh ◽  
E. Robert Burns ◽  
John Yeh ◽  
Hsing-Wu Yeh
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Synergistic Effects ◽  
Rat Kidney ◽  
Transforming Growth Factor Β ◽  
S Phase ◽  
Detectable Effect ◽  
Thymidine Incorporation Assay ◽  
Normal Rat ◽  
Incorporation Assay

The cooperative cell kinetic actions of ET-1 with TGF-α or EGF in normal rat kidney fibroblasts (NRK-49F) and KNRK cells (Kirsten MSV transformed) were analyzed by [3H]-thymidine incorporation assay and flow cytometry. A marked synergistic effect of TGF-α and ET-1 (or EGF and ET-1) on DNA synthesis and G1 to S transition was observed in NRK cells; 15–20% S for TGF-α and 12% S for ET-1 alone but 45–50% S in combination. There was no detectable effect on cell cycle kinetics by TGF-α (1 ng/ml) or EGF (1 ng/ml) plus ET-1 (1 ng/ml) in KNRK cells treated for 22 hours. Insulin, insulin-like growth factor I (IGF-I), fibroblast growth factor (FGF), platelet derived growth factor (PDGF), and transforming growth factor β (TGF-β) were also tested and found to have no significant synergistic effects on ET-1 actions. Our findings suggest that the combination of TGF-α (EGF) and ET-1 is an important part of an intricate network which coordinates progression of G1 to S phase in normal cells.

Changes of serum thyroid hormone levels induce malformations on early embryogenesis in rats

1989 ◽  
Vol 121 (5) ◽  
pp. 739-743 ◽  
Author(s):  
Seijiro Harakawa ◽  
Shoichi Akazawa ◽  
Mihoko Akazawa ◽  
Masumi Hashimoto ◽  
Shunichi Yamashita ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Normal Serum ◽  
Early Embryogenesis ◽  
Rat Embryo ◽  
Thyroid Status ◽  
Rat Serum ◽  
Fetal Malformations ◽  
Normal Rat ◽  
Maternal Thyroid ◽  
Rat Embryo Culture

Abstract. The incidence of malformation is increased in infants of hyperthyroid or hypothyroid woman. Although many papers reported that the fetus is insulted from maternal thyroid hormone, the placenta (maternalfetal barrier) is not yet fully developed before 11.5 days of gestation in rat embryos, suggesting the effect of thyroid hormone on early rat embryogenesis. This study was, therefore, undertaken to investigate whether excess or lack of thyroid hormones would affect early embryogenesis in rat embryo culture. Malformations including open neuropore and microencephaly were observed in 10 of 30 embryos incubated in hyperthyroid serum, and in 12 of 42 cultured in T3-enriched normal serum. Similar malformations were observed in 14 of 42 embryos cultured in hypothyroid serum and in 10 of 30 cultured in hypothyroid serum supplemented with T3. The frequencies of these malformations were significantly higher than in the control embryos (0 in 72 embryos) cultured with normal rat serum. These results suggest that the maternal thyroid status might play an important role for the complication of fetal malformations during early gestational period.

Sign in / Sign up

Export Citation Format

Share Document