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PubMed1967

Thyrocalcitonin and the response to parathyroid hormone.

1) In the absence of the thyroid gland, the infusion of parathyroid hormone leads to a prompt rise in plasma calcium and to prompt increase in the rate of excretion of calcium in the urine.2) In the presence of the thyroid gland, the parathyroid hormone-induced rise in plasma calcium is less marked; the rate of urinary calcium excretion falls initially and rises only after 20 to 30 hours of continuous parathyroid hormone infusion.3) The infusion of exogenous thyrocalcitonin along with the parathyroid hormone into a thyroparathyroidectomized animal leads to a pattern of response similar to that seen in the animal with an intact thyroid gland.4) Thyrocalcitonin has little apparent effect upon the immediate changes in renal function induced by parathyroid hormone.5) We conclude that bone is a major site of action of thyrocalcitonin and that it probably inhibits bone resorption.

Animals↗
PubMed1990

[Secretion of thyrocalcitonin and parathyroid hormone in diffuse polyposis of the colon].

The article presents data obtained in studying the content of calcium regulating hormone thyrocalcitonin and parathyroid hormone in blood plasma of patients with diffuse polyposis of the colon prior to and after a radical surgical treatment. The content of these hormones was also studied in extracts from colonic polyps. The concentration The concentration of thyrocalcitonin was found to decrease after operation. The elevated concentration of thyrocalcitonin was established in polyp extracts which might suggest its "ectopic secretion" in the polyp tissue in diffuse polyposis. Removal of the colon with polyps is followed by normalization of metabolism in the organism which proves the expediency of early surgical treatment.

Adenomatous Polyposis Coli↗
PubMed1993

Decrease in thyrocalcitonin-containing cells and analysis of other congenital anomalies in 11 patients with DiGeorge anomaly.

Experimental studies have demonstrated that the DiGeorge anomaly is due to cranial neural crest abnormalities. In the present study, the quantitation of thyrocalcitonin immunoreactive cells (C-cells) has been used to evaluate whether cells derived from the cranial neural crest are or are not present in normal proportions in patients with this anomaly. Thyroid sections from 11 such patients and 11 control patients were studied immunohistochemically at autopsy in order to determine the number and distribution of thyrocalcitonin-containing cells. Patients with DiGeorge anomaly showed thymic and parathyroid aplasia/hypoplasia and cardiovascular defects, such as type B interrupted aortic arch, truncus arteriosus and tetralogy of Fallot. Other associated defects were alobar holoprosencephaly and meningocele (previously unreported defects in this anomaly), arhinencephaly, renal cystic dysplasia, ureterohydronephrosis, esophageal atresia with tracheoesophageal fistula, and cleft lip and palate. The volume density of C-cells (1.187%) and the mean number of C-cells per follicle (1.42) was significantly lower in patients with DiGeorge anomaly than in control patients (3.475% and 2.367, respectively). These results indicate a decrease in cells derived from the neural crest in patients with DiGeorge anomaly, and support the hypothesis of a neural crest disturbance as the pathogenetic factor responsible for this anomaly.

Calcitonin↗
PubMed1975

The effect of thyrocalcitonin and growth hormones on bone metabolism.

The use of the hormone, thyrocalcitonin, has been shown to change the bone metabolism so that resorption is decreased and calcium increased. The growth hormone seems to add to bone mass and indirectly prevents resorption. The combination of growth hormone and calcitonin seems to cause an unusual amount of resorption. This research has shown that metallic endosteal blade implants are not automatically successful even in short spans with additional support from two abutment teeth. It is true that the type of occlusion of the squirrel monkey is different from that of man, but the prosthetic devices that were placed in these animals can be validly compared to similar devices placed in man. While the hygiene cannot be practiced effectively by the animal, the psychogenic and emotional problems of man offset this disadvantage. Also, the diet of the monkey is not as traumatic to a prosthesis as is man's. Two of the most important criteria for implant success have not proved satisfactory: (1) no pocket depth beyond 3 mm. and (2) negative radiographic pathosis around the implant. While this study was not meant to be one of criticism or evaluation of metallic implants, it should be noted that thyrocalcitonin and the growth hormone, individually used, played an important part in retarding bone resorption around the blade. Autogenous bone grafts for residual alveolar ridge restoration often fail due to rapid osseous resorption and volume loss. The maintenance of osseous elements in the autogenous bone grafts when calcitonin had been administered was quite revealing. This might be the chemotherapeutic basis for the many conditions involving bone that dentists are called upon to treat.

Absorptiometry, Photon↗
PubMed1969

Amino acid sequence of bovine thyrocalcitonin.

Bovine thyrocalcitonin has been isolated in homogeneous form, and its complete amino acid sequence determined. The bovine hormone is a singlechain 32 amino acid polypeptide. It contains a 1-7 amino terminal disulfide bridge, and the carboxyl terminal amino acid is prolinamide. The bovine thyrocalcitonin sequence differs from the porcine sequence by three amino acid residues and from the human sequence by 18 amino acid residues.

Amino Acid Sequence↗
PubMed1967

The effect of thyrocalcitonin on blood-bone calcium equilibrium in the perfused tibia of the cat.

1. In the isolated tibia of the cat, perfused with blood from its own carotid connected to popliteal artery via a pump, infusion of porcine thyrocalcitonin causes an arteriovenous difference in calcium concentration of up to 5%, corresponding to net retention of calcium in bone.2. When taken in conjunction with determinations of radiocalcium clearance in the tibia, the effect is of the right order of magnitude to account for the hypocalcaemic action of thyrocalcitonin in the whole animal.3. Calcium retention was accompanied by a small increase in acidity of outflowing venous blood whereas verification of the hypothesis of calcium regulation by pH change in the bone substance would require a decrease.

Animals↗
PubMed1967

Iodine determined in purified thyrocalcitonin.

Thyrocalcitonin has been suspected of containing iodine, because its analytical behavior and method of extraction are similar to that of iodinated peptides. The iodine content of increasingly pure thyrocalcitonin extracts was determined by two methods, Kolthoff's procedure and activation analysis, with good agreement. A possible link between calcium and iodine metabolism is suggested by these findings.

Amino Acids↗
PubMed1969

Thyrocalcitonin: evidence for physiological function.

A calcium salt given by stomach tube in modest amounts, such as might be ingested in a normal meal, produced hypercalcemia in acutely thyroidectomized fasted rats, whereas in rats with intact thyroid glands the same dose of calcium had little or no detectable effect, presumably because of release of thyrocalcitonin. Thyrocalcitonin apparently protects against hypercalcemia during feeding after deprivation.

Animal Feed↗
PubMed1971

Thyrocalcitonin: stimulation of secretion by pentagastrin.

Administration of a small dose of pentagastrin, a synthetic pentapeptide containing the biologically active portion of the native hormone gastrin, results in a marked, rapid, transitory increase in thyrocalcitonin secretion in the pig. Gastrin or a related gastrointestinal peptide may be important in the physiological secretion of thyrocalcitonin, such as that which occurs when calcium salts are introduced into the gastrointestinal tract.

Animals↗
PubMed1967

Thyrocalcitonin, EGTA, and urinary electrolyte excretion.

The infusion of thyrocalcitonin (TCT) into thyroparathyroidectomized rats, given either no exogenous parathyroid hormone or a constant infusion of this hormone, leads to a transient phosphaturia and a decreased excretion of urinary magnesium, calcium, and hydroxyproline without a change in glomerular filtration rate. The changes in phosphate excretion may be due to a direct effect of the hormone upon renal tubular function or they may be a consequence of the fall in plasma calcium brought about by the action of TCT upon bone. In support of this latter alternative is the fact that the infusion of sodium ethylenebis-oxyethylenenitrilotetraäcetic acid (EGTA, a specific chelator of calcium) also leads to phosphaturia presumably as a consequence of hypocalcemia. However, EGTA infusion leads to enhanced urinary hydroxyproline excretion and sustained phosphaturia. These latter observations are interpreted to mean that alterations in the local ionic environment of osteolytic cells lead to changes in their activity and constitute a local regulatory system whose activity is modulated by the hormones, thyrocalcitonin and parathyroid hormone.

Animals↗
PubMed1979

Spinal cord injury: effect of thyrocalcitonin on periarticular bone formation in three subjects.

Sodium fluoride 18F scintimetry was performed before and after 1 month of salmon thyrocalcitonin treatment of 3 spinal cord injured patients with periarticular ossification of the hips and knees. Thyrocalcitonin therapy caused a marked diminution of 18F uptake in 1 patient with long-standing periarticular bone of both hips. Clinically, the range of motion in this subject increased by 25 degrees and there was a marked decrease in pain locally. The results were, however, not duplicated in the 2 patients with periarticular bone formation of short duration.

Adult↗
PubMedDate not supplied

[Effect of prolonged administration of thyrocalcitonine on mineralization of regenerating bone after fracture].

A distinct effect on all the stages of regenerating bone mineralisation was observed after daily (within the experimental period) intramuscular administration of thyrocalcitonine with prolonged action (a complex with polyvinyl pyrrolidone) into male rat at a dose 2.5 un/kg of body weight. The drug caused an inhibitory effect on metabolism within the first 10 days of the experiment. Within 2-3 weeks after the fracture the intensity of metabolic processes was increased. Contents of calcium, phosphorus, sodium and potassium were markedly increased in liquid phase of the bone rissue. The synthesis of phosphoproteins, organic non-protein phosphates and the inorganic phosphate was also increased. The data obtained suggest that thyrocalcitonine caused a stimulating effect on aerobic resynthesis of macroergic phosphate containing substances and the increase in the functional activity of osteogenic cells.

Animals↗
PubMed1978

[Effect of thyrocalcitonin on the functions of the intact and hypertrophied myocardium].

Examination of 20 individuals without any pathological conditions of the cardiovascular system and 8 patients with myocardial hypertrophy has shown that the hypocalciemic hormone of the thyroid gland thyrocalcitonin has a certain negative inotropic effect and does not possess chrono- and dromotropic affects. The mechanism of the cardiac effect of thyrocalcitonin is evidently due to its effect on the metabolism of calcium and its transportation in the myocardial structures.

Adult↗
PubMed1978

[Participation of thyrocalcitonin in the development of stress].

The immobilization stress in rats entailed raise of calcium content in the plasma followed by a decrease to the hypocalcaemic level. The thyrocalcitonin activity of plasma was undetectable in intact rats, but increased to 5 mU/ml after 3 hrs of stress. Administration of bovine thyrocalcitonin (10 U/100 g) before the immobilization inhibited the lowering of CRF activity of hypothalamic extracts, ACTH content of hypophysis, and ascorbic acid concentration in adrenal glands of the rats under stress, i.e. inhibited the development of stress reaction.

Adrenocorticotropic Hormone↗
PubMed1975

[Exocrine pancreatic function and calcium balance. Experimental studies of the effect of parathyroid hormone, vitamin D3, 25-hydroxycholecalciferol, dihydrotachysterin and thyrocalcitonin (author's transl)].

The effect of the acute elevation of extracellular calcium concentration, of vitamin D3, 25-hydroxycholecalciferol, dihydrotachysterin, parathyroid hormone and of thyrocalcitonin on the exocrine function of the perfused cat pancreas was studied. Elevation of the perfusate calcium concentration resulted in an initial increase in the enzyme and, occasionally, calcium concentration of the pancreatic juice, the flow rate and the secretion of magnesium and chloride were not very much altered. The application of vitamin D3 and 25-hydroxycholecalciferol elevated the stimulated (by acetylcholine or cholecystokinin-pancreocymin) protein and enzyme output (lipase, alpha-amylase). Parathyroid hormone and, especially, thyreocalcitonin inhibited the stimulated protein and enzyme secretion, volume and rate of the electrolyte secretion were not changed. In states of calcium excess the stimulated protein output was decreased by both vitamin D3 and parathyroid hormone.

Acetylcholine↗
PubMed1975

Hypercalcemic effect of catecholamines and its prevention by thyrocalcitonin.

Earlier work by others has shown that the catecholamines, epinephrine and isoproterenol, can raise blood calcium levels in parathyroidectomized but not intact rats, and can restrict the hypocalcemic effect of injected thyrocalcitonin (TCT). The present findings support this earlier work, further showing that such catecholamines can produce hypercalcemia in rats after removal of the thyroid gland by acute thyroparathyroidectomy (TPTX) and indicating that these drugs may raise blood calcium by mobilizing calcium from bone. Rats were fasted overnight, subjected to TPTX and concurrently injected with adrenergic agonist or antagonist drugs alone or in combination. Epinephrine, isoproterenol, and the beta-2 adrenergic agonist, salbutamol, in doses greater than or equal to 1 mg/kg raised blood calcium from low normal levels (approximately 9-10 mg/100 ml) by 1.5 to 2 mg/100 ml (p less than 0.01). Hypercalcemia was apparent by 1 hour after injection and lasted for 1-4 hours. The extent of Ca elevation was dose-related. Pretreatment of rats with the alpha-adrenergic antagonist, phenoxybenzamine, enhanced the effect of epinephrine while pretreatment with the beta-antagonist, propranolol, reduced the effect of isoproterenol. The more selective beta-2 antagonist, butoxamine, but not the beta-1 antagonist, practolol, also reduced the hypercalcemic effect of isoproterenol in TPTX rats. These results suggest that catecholamine-induced hypercalcemia in TPTX rats is mediated by beta-2 adrenergic receptors. Related studies using rats prelabeled with 45Ca further suggest that the catecholamines, like parathyroid hormone, may act to raise blood calcium by mobilizing calcium from bone. The fact that these catecholamines could induce marked hypercalcemia in acutely TPTX rats but not in intact rats indicated that endogenous TCT protects the thyroid intact rat against hypercalcemia. The present findings support this idea in showing that isoproterenol and salbutamol raised levels of immunoreactive rat TCT in both thyroid venous and peripheral blood. Catecholamines apparently can promote TCT secretion, either directly or by a small transient increase in blood calcium. This, in turem, acts to combat hypercalcemia in thhroid-intact rats.

Albuterol↗
PubMed1996

Interleukin-1 beta and tumor necrosis factor-alpha production by human monocytes cultured with L-thyroxine and thyrocalcitonin: relation to severe root shortening.

The objectives of this study were to determine whether L-thyroxine (T4) and thyrocalcitonin (TCA) influence monocyte production of interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) and to examine IL-1 beta and TNF-alpha production in monocytes from a group of orthodontic patients with severe root shortening. Human monocytes were incubated with varying concentrations of T4 and TCA for 24 hours, and IL-1 beta and TNF-alpha levels were measured by ELISA. At a concentration of 0.1 microgram/ml, T4 and TCA induced significantly more IL-1 beta than untreated controls, and T4 induced more IL-1 beta than TCA. Neither hormone induced significant TNF-alpha release, conversely, TCA had an inhibitory effect on unstimulated monocyte release of TNF-alpha. TCA was also shown to inhibit, but not reverse, the activational effect of lipopolysaccharide on monocyte TNF-alpha release. T4 and TCA concentrations as low as 0.1 pg/ml caused monocytes to release significant amounts of IL-1 beta. The highest concentration of T4 tested (1.0 microgram/ml) induced significantly less IL-1 beta production than lower concentrations. T4- and TCA-treated monocytes bound more labeled IL-1 beta than untreated controls, which suggests that these hormones increase IL-1 receptor expression. There was a wide range of unstimulated and stimulated IL-1 beta and TNF-alpha production by root resorption subject monocytes with no significant differences between resorption and nonresorption group means. This data suggest that patient monocytes did not differ from control monocytes in regard to these cytokine parameters, and therefore in vitro IL-1 beta and TNF-alpha levels could not distinguish resorption subjects.

Adult↗