scholarly journals In Vitro and In Vivo Refractoriness to Thyrotropin Stimulation of Iodine Organification and Thyroid Hormone Secretion

1979 ◽  
Vol 64 (1) ◽  
pp. 265-271 ◽  
Author(s):  
James B. Field ◽  
Andrew Dekker ◽  
Gail Titus ◽  
Mary Eleanor Kerins ◽  
William Worden ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Hormone Secretion ◽  
Stimulation Of

In vivo effects of flavonoid EMD 21388 on thyroid hormone secretion and metabolism in rats

1991 ◽  
Vol 261 (2) ◽  
pp. E227-E232 ◽  
Author(s):  
J. P. Schroder-van der Elst ◽  
D. van der Heide ◽  
J. Kohrle
Keyword(s):  
Thyroid Hormone ◽  
Hormone Secretion ◽  
Male Rats ◽  
Intact Male ◽  
Hormone Production ◽  
Iodide Uptake ◽  
Brown Adipose ◽  
In Vivo Effects

In vitro, the synthetic flavonoid EMD 21388 appears to be a potent inhibitor of thyroxine (T4) 5'-deiodinase and diminishes binding of T4 to transthyretin. In this study, in vivo effects of long-term administration of EMD 21388 on thyroid hormone production and metabolism were investigated. Intact male rats received EMD 21388 (20 mumol.kg body wt-1.rat-1.day-1) for 14 days. [125I]T4 and 3,5,3'-[131I]triiodotyronine (T3) were infused continuously and intravenously in a double-isotope protocol for the last 10 and 7 days, respectively. EMD 21388 decreased plasma thyroid hormone concentrations, but thyrotropin levels in plasma and pituitary did not change. Plasma clearance rates for T4 and T3 increased. Thyroidal T4 secretion was diminished, but T3 secretion was elevated. Extrathyroidal T3 production by 5'-deiodination was lower. T4 concentrations were markedly lower in all tissues investigated. Total tissue T3 was lower in brown adipose tissue, brain, cerebellum, and pituitary, tissues that express the type II 5'-deiodinase isozyme due to decreased local T3 production. Most tissues showed increased tissue/plasma ratios for T4 and T3. These results indicate that this flavonoid diminished T4 and increased T3 secretion by the thyroid, probably in analogy with other natural flavonoids, by interference with one or several steps between iodide uptake, organification, and hormone synthesis.

scholarly journals Obestatin Partially Affects Ghrelin Stimulation of Food Intake and Growth Hormone Secretion in Rodents

Endocrinology ◽  
2007 ◽  
Vol 148 (4) ◽  
pp. 1648-1653 ◽  
Author(s):  
Philippe Zizzari ◽  
Romaine Longchamps ◽  
Jacques Epelbaum ◽  
Marie Thérèse Bluet-Pajot
Keyword(s):  
Food Intake ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Male Rats ◽  
Pituitary Cells ◽  
Gh Secretion ◽  
Freely Moving ◽  
Stimulation Of

Administration of ghrelin, an endogenous ligand for the GH secretagogue receptor 1a (GHSR 1a), induces potent stimulating effects on GH secretion and food intake. However, more than 7 yr after its discovery, the role of endogenous ghrelin remains elusive. Recently, a second peptide, obestatin, also generated from proteolytic cleavage of preproghrelin has been identified. This peptide inhibits food intake and gastrointestinal motility but does not modify in vitro GH release from pituitary cells. In this study, we have reinvestigated obestatin functions by measuring plasma ghrelin and obestatin levels in a period of spontaneous feeding in ad libitum-fed and 24-h fasted mice. Whereas fasting resulted in elevated ghrelin levels, obestatin levels were significantly reduced. Exogenous obestatin per se did not modify food intake in fasted and fed mice. However, it inhibited ghrelin orexigenic effect that were evident in fed mice only. The effects of obestatin on GH secretion were monitored in superfused pituitary explants and in freely moving rats. Obestatin was only effective in vivo to inhibit ghrelin stimulation of GH levels. Finally, the relationship between octanoylated ghrelin, obestatin, and GH secretions was evaluated by iterative blood sampling every 20 min during 6 h in freely moving adult male rats. The half-life of exogenous obestatin (10 μg iv) in plasma was about 22 min. Plasma obestatin levels exhibited an ultradian pulsatility with a frequency slightly lower than octanoylated ghrelin and GH. Ghrelin and obestatin levels were not strictly correlated. In conclusion, these results show that obestatin, like ghrelin, is secreted in a pulsatile manner and that in some conditions; obestatin can modulate exogenous ghrelin action. It remains to be determined whether obestatin modulates endogenous ghrelin actions.

scholarly journals Effect of exogenous glucocorticoid on osmotically stimulated antidiuretic hormone secretion and on water reabsorption in man

2006 ◽  
Vol 155 (6) ◽  
pp. 845-848 ◽  
Author(s):  
Volker Bähr ◽  
Norma Franzen ◽  
Wolfgang Oelkers ◽  
Andreas F H Pfeiffer ◽  
Sven Diederich
Keyword(s):  
Antidiuretic Hormone ◽  
Water Deprivation ◽  
Hormone Secretion ◽  
Water Reabsorption ◽  
Glucocorticoid Treatment ◽  
Osmotic Stimulation ◽  
Before And After ◽  
Stimulation Of

Objective: Glucocorticoids exert tonic suppression of antidiuretic hormone (ADH) secretion. Hypocortisolism in secondary adrenocortical insufficiency can result in a clinical picture similar to the syndrome of inappropriate ADH secretion. On the other hand, in vitro and in vivo results provide evidence for ADH suppression in states of hypercortisolism. To test the hypothesis that ADH suppression is of relevance during glucocorticoid therapy, we investigated the influence of prednisolone on the osmotic stimulation of ADH. Design and methods: Seven healthy men were subjected to water deprivation tests with the measurement of plasma ADH (pADH) and osmolality (posmol) before and after glucocorticoid treatment (5 days 30 mg prednisolone per day). Results: Before glucocorticoid treatment, the volunteers showed a normal test with an adequate increase of pADH (basal 0.54 ± 0.2 to 1.9 ± 0.72 pg/ml (mean ± S.D.)) in relation to posmol(basal 283.3 ± 8.5 to 293.7 ± 6 mosmol/kg). After prednisolone intake, pADH was attenuated (<0.4 pg/ml) in spite of an increase of posmol from 289.3 ± 3.6 to 297.0 ± 5.5 mosmol/kg. However, urine osmolar concentration increased normally during water deprivation after prednisolone. Urinary cAMP excretion increased during water deprivation without glucocorticoid treatment from 3.56 ± 0.55 to 6.07 ± 0.76 μmol/l, reflecting the increased pADH levels. The rise in cAMP excretion was completely blunted by prednisolone treatment. Conclusions: We speculate that there may be an ADH-independent stimulation of the formation or function of aquaporin-2 channels by prednisolone and/or a direct osmotic stimulation of water reabsorption independent of ADH and glucocorticoid control.

THE SEROTONIN RETAINING EFFECT OF LITHIUM IN THE RAT THYROID

1976 ◽  
Vol 82 (2) ◽  
pp. 530-534 ◽  
Author(s):  
H. Vejlsted ◽  
O. Korsgaard
Keyword(s):  
Thyroid Hormone ◽  
Inhibitory Action ◽  
Hormone Secretion ◽  
Serotonin Release ◽  
Hormone Release ◽  
Rat Thyroid ◽  
Stimulation Of

ABSTRACT The hypothesis of a lithium induced serotonin retention in the rat thyroid has been tested. It has been found that the thyroid in rats treated with lithium contains double the amount of serotonin compared with glands from untreated animals. The ability of TSH to stimulate serotonin release is inhibited by lithium. The ability of serotonin to stimulate thyroid hormone secretion in vitro is documented. The inhibitory action of lithium on both TSH and serotonin stimulation of hormone release is documented. The serotonin retaining effect of lithium as part of the goitrogenic effect of this ion is discussed.

ACTION OF POTASSIUM IODIDE ON THYROID ACID PROTEASE

1973 ◽  
Vol 74 (4) ◽  
pp. 703-710 ◽  
Author(s):  
M. A. Pisarev ◽  
N. Altschuler
Keyword(s):  
Thyroid Hormone ◽  
Potassium Iodide ◽  
Enzyme Preparation ◽  
Specific Activity ◽  
Hormone Secretion ◽  
Enzyme Synthesis ◽  
Acid Protease ◽  
Rule Out ◽  
Stimulation Of

ABSTRACT Potassium iodide (KI) is known to inhibit thyroid hormone secretion. In the present studies its action on the proteolytic step of this process was investigated. Rats were treated with KI (200 μg/ml in the drinking water) for 30 days. This treatment caused a decrease of protease activity in total homogenate and in the specific activity of a 15 000 × g pellet. No alteration in the pattern of subcellular distribution was observed. In order to rule out an action of KI on enzyme activity its in vitro action was studied. KI concentrations around 103-–10−4 m were without effect, though 10−2 caused a stimulation of activity. Similar results were observed when a liver enzyme preparation was checked under the same conditions. Neither CL− nor F− had an effect on thyroid or liver protease at concentrations between 10−2 to 10−4 m. The present results suggest that KI inhibition of thyroid hormone secretion can be explained at least in part by its action on acid protease. Moreover, the lack of an in vitro inhibitory affect of KI would suggests that this drug affects enzyme synthesis and/or breakdown.

Thrombopoietin-Induced Stimulation of Megakaryocyte- Enriched Bone Marrow Cultures

1979 ◽  
Author(s):  
K. L. Kellar ◽  
B. L. Evatt ◽  
C. R. McGrath ◽  
R. B. Ramsey
Keyword(s):  
Bone Marrow ◽  
Dna Synthesis ◽  
Bone Marrow Cells ◽  
Rabbit Plasma ◽  
Bone Marrow Cultures ◽  
Plasma Fractions ◽  
Marrow Cultures ◽  
Stimulation Of

Liquid cultures of bone marrow cells enriched for megakaryocytes were assayed for incorporation of 3H-thymidine (3H-TdR) into acid-precipitable cell digests to determine the effect of thrombopoietin on DNA synthesis. As previously described, thrombopoietin was prepared by ammonium sulfate fractionation of pooled plasma obtained from thrombocytopenic rabbits. A control fraction was prepared from normal rabbit plasma. The thrombopoietic activity of these fractions was determined in vivo with normal rabbits as assay animals and the rate of incorporation of 75Se-selenomethionine into newly formed platelets as an index of thrombopoietic activity of the infused material. Guinea pig megakaryocytes were purified using bovine serum albumin gradients. Bone marrow cultures containing 1.5-3.0x104 cells and 31%-71% megakaryocytes were incubated 18 h in modified Dulbecco’s MEM containing 10% of the concentrated plasma fractions from either thrombocytopenic or normal rabbits. In other control cultures, 0.9% NaCl was substituted for the plasma fractions. 3H-TdR incorporation was measured after cells were incubated for 3 h with 1 μCi/ml. The protein fraction containing thrombopoietin-stimulating activity caused a 25%-31% increase in 3H-TdR incorporation over that in cultures which were incubated with the similar fraction from normal plasma and a 29% increase over the activity in control cultures to which 0.9% NaCl had been added. These data suggest that thrombopoietin stimulates DNA synthesis in megakaryocytes and that this tecnique may be useful in assaying thrombopoietin in vitro.

scholarly journals Contamination of erythropoietin by endotoxin: in vivo and in vitro effects on murine erythropoiesis

Blood ◽  
1979 ◽  
Vol 54 (1) ◽  
pp. 146-158 ◽  
Author(s):  
KS Zuckerman ◽  
PJ Quesenberry ◽  
J Levin ◽  
R Sullivan
Keyword(s):  
Significant Inhibition ◽  
Erythropoietic Activity ◽  
Limulus Amebocyte Lysate ◽  
Endogenous Erythropoietin ◽  
Significant Change ◽  
In Vitro Effects ◽  
Stimulation Of

Abstract Endotoxin was detected in all erythropoietin preparations tested and was removed from four lots, without loss of erythropoietic activity, by adsorption with limulus amebocyte lysate. Comparison of adsorbed (endotoxin-depleted) and nonadsorbed (endotoxin-containing) erythropoietin preparations demonstrated significant inhibition of CFU- e and BFU-e in vitro by nonadsorbed erythropoietin at concentrations higher than 0.25 U/ml and 2.0 U/ml, respectively. CFU-e and BFU-e were inhibited significantly by readdition in vitro of 10(-5)-10(-3) mug of endotoxin per unit of limulus-adsorbed erythropoietin. Administration of saline or 6 U of nonadsorbed or adsorbed erythropoietin twice a day for 4 days of CF1 mice resulted in reticulocyte counts of 2.1%, 9.9%, and 15.9%, respectively. Nonadsorbed erythropoietin resulted in a 29% decrease in erythropoiesis, a 42% decrease in CFU-e, and a 16% increase in granulopoiesis in the marrow, whereas adsorbed erythropoietin caused a 28% increase in erythropoiesis, no significant change in CFU-e and a 19% decrease in granulopoiesis in the marrow. Both preparations resulted in marked increases in splenic erythropoiesis and granulopoiesis. The effects of adsorbed erythropoietin are similar to those produced following stimulation of hematopoiesis by endogenous erythropoietin. Hemopoietic changes induced by nonadsorbed erythropoietin in vivo and in vitro are affected substantially by contamination of the erythropoietin preparations with endotoxin.

Effects of α-adrenoceptor agonists and antagonists on thyroid hormone secretion

1985 ◽  
Vol 108 (2) ◽  
pp. 184-191 ◽  
Author(s):  
Bo Ahrén
Keyword(s):  
Thyroid Hormone ◽  
Dose Level ◽  
Hormone Secretion ◽  
High Dose ◽  
Inhibitory Effects ◽  
High Dose Level ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists

Abstract. The effects of various α-adrenoceptor agonists and antagonists on blood radioiodine levels were studied in mice pre-treated with 125I and thyroxine. The non-selective α-adrenoceptor agonist noradrenaline and the selective α1-adrenoceptor agonist phenylephrine both enhanced blood radioiodine levels. Noradrenaline was more potent than phenylephrine. Contrary, the selective α2-adrenoceptor agonist clonidine depressed basal levels of blood radioiodine. The non-selective α-adrenoceptor antagonist phentolamine and the selective α1-adrenoceptor antagonist prazosin both inhibited the noradrenaline-induced elevation of radioiodine levels, whereas the α2-adrenoceptor antagonist yohimbine had no such effect, except at a high dose level. All three α-adrenoceptor agonists, noradrenaline, phenylephrine and clonidine, inhibited the radioiodine response to TSH. In addition, TSH-induced increase in radioiodine levels was inhibited by prazosin, whereas yohimbine had no effect. Phentolamine inhibited the radioiodine response to TSH when given 2 h prior to TSH, whereas when given 15 min prior to TSH the response to TSH was potentiated by Phentolamine. It is concluded, that under in vivo conditions in the mouse, α1-adrenoceptor activation stimulates basal thyroid hormone secretion and inhibits TSH-induced thyroid hormone secretion. Further, α2-adrenoceptor activation inhibits basal thyroid hormone secretion. In addition, TSH-induced thyroid hormone secretion is inhibited by α1-adrenoceptor antagonism. Thus, α-adrenoceptors induce both stimulatory and inhibitory effects of thyroid function.

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