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L Gozariu

Publications and source records attributed to L Gozariu.

At least 19 recordsLinked to original sources
PubMed2003

The effects of triiodothyronine on human osteoblast-like cells metabolism and interactions with growth hormone.

The expression of thyroid hormones receptors in osteoblasts and osteoclasts has involved these cells as direct targets for triiodothyronine (T3), but thyroid hormones may also interact with other hormones or local growth factors to exert their actions on bone cells. Among these, growth hormone (GH) is recognised as participating in the acquisition and maintenance of bone mass and exerting stimulatory effects on human osteoblastic cells. The aim of this study was to investigate T3 effects on primary human adult osteoblast-like cells (HOB) as well as to test for possible interactions between T3 and GH on bone cell metabolism. Primary human bone cell cultures were obtained by outgrowth from trabecular bone fragments from the hip and knee. Dose-response studies demonstrated enhanced [3H]-thymidine incorporation for T3 at 10(-9), 10(-8), 10(-7) and 20(-7) M, with a maximal response of 162.81 +/- 12.97 % with T3 10(-8) M, compared to vehicle (p < 0.001). Time-course studies showed an increased osteoblast-like cell proliferation after 24 h, followed by a decrease of cell proliferation by 48 h and 72 h of culture, respectively, when compared to control cells, with a maximal response after 72 h (T3 10(-10) M: 45.21 +/- 6.97 %, p < 0.01). In addition, T3 markedly increased specific alkaline phosphatase (AP) activity in HOB (10(-10) M: 169.86 +/- 12.14 % vs. control, p < 0.001), but no significant influence on type I procollagen propeptide (PICP) production was observed. At 10(-9) - 10(-7) g/ml, GH significantly enhanced HOB proliferation (p < 0.001) however, GH effects were not dose-dependent. Triiodothyronine, at a high concentration (10(-7) M), stimulated GH-receptor (GHR) mRNA levels by 165.20 +/- 16.54 % after 24 h (p < 0.05). Correspondingly, a synergistic effect of T 3 with the same concentration and GH on cell proliferation in human adult osteoblast-like cells was found.

Adult↗
PubMed2001

Effects of triiodothyronine on the insulin-like growth factor system in primary human osteoblastic cells in vitro.

Thyroid hormone plays a major role in the regulation of bone metabolism but the mechanism by which this is accomplished is not clear. Interactions of thyroid hormone with the growth hormone/insulin-like growth factors (IGFs) axis suggest an alternate pathway of action for triiodothyronine (T(3)) on bone formation, besides direct effects. The present study investigates the influence of T(3) on IGF-1, IGF-2, IGF-1 receptor (IGF-1R), and IGF binding protein (IGFBP) transcripts, and on IGF-1 action in human osteoblastic cells (hOB) under serum-free culture conditions. No influence of T(3) on IGF-1, IGF-2, IGFBP-3, or IGFBP-4 mRNA levels in hOB was observed. However, T(3) at concentrations of 10(-8) mol/L and 10(-7) mol/L increased IGF-1R mRNA levels in a dose-dependent manner (p < 0.01) and enhanced IGFBP-5 mRNA levels at a concentration of 10(-7) mol/L (p < 0.05), as assessed by reverse transcriptase-polymerase chain reaction. Correspondingly, Scatchard analysis of [(125)I]-IGF-1 binding revealed that T(3) at 10(-7) mol/L increased the number of IGF-1 binding sites in hOB, with small changes in receptor affinity. In addition, a synergistic effect of T(3) and IGF-1 on hOB proliferation was found (p < 0.05). We conclude that IGF-1R and IGFBP-5 are thyroid hormone target genes in human osteoblasts, whereas IGF-1 mRNA expression itself appears not to be regulated by T(3) in hOB. However, T(3) stimulates IGF-1R mRNA expression as well as IGF-1 binding and IGF-1 induced cell proliferation in osteoblasts, thus suggesting thyroid hormone may potentiate the effect of IGF-1 at the receptor level. This may contribute to the positive effects of thyroid hormone on bone formation, which, in addition, may be modulated by increased IGFBP-5 expression.

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PubMed1999

Effects of parenteral pharmacological magnesium loading on insulin secretion in experimental thyrotoxicosis.

Thyrotoxicosis is characterised by decreased magnesium pool and also insulin resistance. The present study is evaluating the parameters of glucose metabolism under pharmacological magnesium loading in experimentally induced thyrotoxicosis, in rats. Insulin secretion was significantly increased in thyrotoxicosis compared to controls, expressing probably the status of insulin resistance due to thyroxine excess. After intraperitoneal magnesium infusion, plasma magnesium reached pharmacologically high concentrations and insulin secretion decreased significantly, but this decrease was not accompanied by alterations of glucose homeostasis. In controls, we also found a tendency towards the decrease of insulin secretion after magnesium loading, but it did not reach statistical significance. Thus, insulin secretion seems more sensitive to the inhibitory effects of magnesium overload in experimental thyrotoxicosis.

Animals↗
PubMed1993

The mechanism involved in the central effect of 5-leu enkephalin on the calcitonin secretion.

Calcitonin (CT) secretion is not exclusively under the control of calcium levels in the plasma, but also depends on the sympathetic-adrenergic tone. In previous experiments we stressed out the possible role played by 5-leu enkephalin (5-LE) in the nervous regulation of the CT secretion. Intracerebroventricular (i.c.v.) 5-LE in doses of 100 micrograms could act at a central level through a mechanism independent from the noradrenergic pathways, since i.c.v. 6-OHDA and propranolol could not interfere with its stimulatory effect on the CT content of the thyroid. In the present experiments, performed in anaesthetized Wistar-Bratislava rats, we studied the involvement of mu and delta receptors in the central effect of 5-LE on the CT content of the thyroids and the CT levels in the plasma. These parameters were measured in parallel, by means of a competitive radioimmunoassay with double antibodies (Peninsula Lab.). 5-LE probably bound to both mu and delta receptors, since its effect on the CT secretion was reversed by 13 micrograms of naloxone (i.c.v.). A partial blockade, comparable to naloxone, was noticed after 382 micrograms of CTOP (i.c.v.), a specific antagonist of the mu receptors--stressing out their involvement in the stimulatory effect of 5-LE on the CT secretion. 250 Ug of ICI 174864 (i.c.v.), a selective antagonist the the delta receptors completely blocked the stimulation induced by 5-LE on the CT secretion to values significantly lower as compared to the controls and even to the sympathectomized group. This suggests the tonic role played by enkephalins in the CT secretion, through the central activation of delta receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Inhibitory role of somatostatin on calcitonin secretion.

Calcitonin (CT) secretion is not exclusively controlled by calcemia, but the secretory tonus is maintained by the beta-stimulatory adrenergic system Somatostatin (SMS) plays a neuromodulatory role with the reduction of CT secretion by its interference at the central and peripheral level of the beta adrenergic receptors. The experiments were carried out on groups of rats in which the effect of SMS on CT content of the thyroid gland was followed up. Thus, SMS administered i.c.v. significantly reduced the basal CT secretion without blocking the stimulatory effect of calcium. The results were comparable with those obtained after the blockade of the sympatho-adrenergic system by chemical sympathectomy with 6HODA or propranolol. Central blockade of alpha receptors with phentolamine determined a significant rise of CT. This effect was annihilated by SMS. The i.v. administration of SMS did not induce a change in CT content of the thyroid, but blocked the stimulatory action of hypercalcemia. The results are identical with those obtained by blocking the beta-receptors with propranolol. SMS also blocked the stimulatory effects of isoproterenol on CT secretion. The data obtained revealed the fact that SMS lowers CT secretion by the central and peripheral interference of the sympatho-adrenergic path, maintaining the secretory tonus of the thyroid C cells.

Animals↗
PubMed1991

Insulin secretion in magnesium silicate-induced osteopenia in rats.

Local inflammation induced in rats by subcutaneous injection of magnesium silicate is followed by general metabolic, endocrine and immune reactions. Three weeks after inflammation induction, important bone loss, inflammation-mediated osteopenia (IMO) were found. The study proposes to investigate if IMO influences endogenous insulin secretion and if insulin therapy modifies the amount of bone loss, knowing its osteoprotective effect. Experiments were carried out on adult rats, three weeks after local inflammation induction. Baseline glucose and insulin levels did not change as compared to controls. After glucose stimulation, insulinogenic index decreased in the IMO group, which evidences decrease of insulin secretion. Insulin treatment initiated at the same time with IMO did not induce significant changes as regards the response to glucose tolerance test. However, bone calcium was increased as compared to the untreated IMO group, without reaching the control level.

Animals↗
PubMed1986

Late hypothyroidism following subacute thyroiditis.

The authors followed up the incidence of permanent hypothyroidism in 35 patients with subacute thyroiditis (SAT) in their past history. The investigations were made one to four years after the acute episode. Ten of these presented repeated recurrences despite the therapy with glucocorticoids. The investigations included serum determination by RIA of T4, T3, TSH and thyroglobulin as well as of circulating thyroid antibodies. Permanent hypothyroidism subsequent to SAT occurred in two patients. In one of them it occurred following thyroid surgery performed for repeated recurrences. Both patients presented high levels of circulating thyroglobulin antibodies suggesting a possible transition to autoimmune thyroiditis. In the authors' opinion permanent hypothyroidism is likely to develop after SAT only in association with an autoimmune process or after thyroid surgery.

Adult↗
PubMed1976

Thyroparathyroid conditioning of hydrocortisone and glucagon-induced hypocalcemic effect in rats.

A single dose of 2.5 mg hydrocortisone induced hypocalcemia in both intact and parathyroidectomized rats. This effect disappeared in the thyroparathyroidectomized group and did not reappear after the substitution with parathormone. A single dose of 0.2 mg glucagon produced a significant hypocalcemic effect in intact, but not in parathyroidectomized rats. In the latter group, however, the hypocalcemic effect of glucagon reappeared after the administration of parathormone. It was concluded that the hypocalcemic effect of hydrocortisone may be conditioned by the presence of calcitonin secreting thyroid and that of glucagon - by the presence of parathyroids.

Animals↗