PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Thyroid Effects”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1986

Beta-endorphin and its congeners in rat pituitary and thyroid: effects of propylthiouracil and thyroid hormone administration.

Immunoreactive beta-endorphin (ir-beta EP) and immunoreactive N-acetyl-endorphin (ir-NacEP) have been demonstrated in the rat thyroid by specific RIA and characterized by reverse phase HPLC. In addition, pituitary and thyroid ir-beta EP and ir-NacEP levels have been determined after manipulation of the pituitary-thyroid axis by chronic (21 days) treatment with 1) propylthiouracil (PTU), 2) L-T4, 3) L-T3, or 4) T3 plus PTU. No difference in anterior pituitary or neurointermediate lobe ir-beta EP was seen between controls and treated groups (n = 8/group). In contrast, levels of ir-NacEP were markedly lower (P less than 0.01) in both hypo- and hyperthyroid groups than in controls, in both anterior pituitary and neurointermediate lobe. In the thyroid, levels of both ir-beta EP and ir-NacEP were profoundly depressed (P less than 0.01) in all treated groups, with no change in calcitonin levels, suggesting that the thyroid effect of PTU and T3/T4 may be specific for the synthesis, processing, and/or release of pro-opiomelanocortin derived peptides. The findings in this study suggest 1) that acetylation of pituitary and thyroid beta EP is similarly sensitive to PTU and thyroid hormone administration and 2) that in the thyroid, but not in the pituitary, both PTU and thyroid hormones markedly lower levels of pro-opiomelanocortin-derived peptides.

Acetylation↗
PubMed1986

Graves' disease and Hashimoto's thyroiditis: effects of high doses of antithyroid drugs on thyroid autoantibody levels.

We studied the effects of high doses of methimazole (MMI) or propylthiouracil (PTU) on thyroid-stimulating antibody (TSAb), antithyroid microsomal (MCHA) and antithyroglobulin (TGHA) levels in Graves' disease and Hashimoto's thyroiditis. Thirty Graves' hyperthyroid patients were treated for 14 +/- 8 months (mean +/- SD) with MMI, 60-80 mg daily or PTU, 900-1200 mg daily plus T3, 50-75 micrograms daily. Fifteen Hashimoto's thyroiditis patients (4 of whom hypothyroid) received 100-200 micrograms of T4 daily for 4-8 weeks prior to MMI, 60-90 mg daily or PTU, 900 mg daily for 12-16 weeks. In Graves' disease a decrease (p less than 0.001) in TSAb activity (20/25 patients) was observed: before therapy, 0.424 +/- 0.506 pmoles/mg wet wt and at the end of treatment, 0.189 +/- 0.23 pmoles/mg wet wt. The MCHA titers also fell (18/26 patients) from 1:10,403 +/- 20,197 to 1:3,476 +/- 5,252 (p less than 0.01) and was associated with a decrease in free T4 values (1.23 +/- 0.69 vs. 0.51 +/- 0.36 ng/dl; p less than 0.01). A fall of MCHA titers in T4-treated Hashimoto's thyroiditis patients (1:10,416 +/- 25,576) was found when compared with the value before T4 (1:25,920 +/- 39,973; p less than 0.001). However, the titers of MCHA (1:13,280 +/- 25,992) did not change on MMI or PTU plus T4 treatment. The TGHA titers fell in a single patient. No alterations were observed in serum immunoglobulins. Serum concentrations of the complement factor C'3 remained higher (p less than 0.01) than normal values in both Graves' disease and Hashimoto's thyroiditis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Epidermal growth factor (EGF) inhibits the secretomotor response of the thyroid: effects of EGF on radioiodine turnover and fluid transport in cultured porcine thyroid cells.

Thyrotrophin (4-256 microU/ml) promoted an increase in the rate of release of radioiodine from the organic iodine pool of cultured porcine thyroid cells in follicular formations. This action of TSH was antagonized by low concentrations of epidermal growth factor (EGF; 0.1-5 nmol/l). The maximal effect of EGF was reached by 0.5 nmol/l. EGF (0.5-5 nmol/l) also inhibited the stimulatory effect of 8-chloro cyclic AMP (0.06-1.0 nmol/l) on radioiodine turnover. Exposure of thyroid cultures to media with a calcium concentration of 17.7 mumol/l (1% of normal) resulted in a very marked increase in the rate of release of radioiodine. The effect of TSH in low-calcium media was to inhibit the increased release of radioiodine, and EGF (0.5 nmol/l) antagonized this inhibitory effect of TSH. The calcium ionophore, A23187, stimulated radioiodine release in a dose-dependent fashion, and EGF (1.7 nmol/l) inhibited this response. Fluid transport in thyroid monolayers was stimulated by prostaglandin E2 (PGE2; 1 mumol/l). EGF (5 nmol/l) also stimulated fluid transport, but antagonized the effect of PGE2 added subsequently. It was concluded that EGF exerted acute antagonistic effects on thyroid cell responses in vitro to cyclic AMP and agents promoting accumulation of cyclic AMP in time-frames too short for these inhibitory effects to be attributable to the dedifferentiative effect of the growth factor.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1985

Thyroid iodine content and serum thyroid hormone levels in autoimmune thyroiditis: effect of iodide supplementation.

The relationship between thyroid iodine content (TIC) measured by x-ray fluorescence and serum TSH, T4, and T3 levels was investigated under iodide supplementation (0.5 mg/day for 1 to 9 mo). In five euthyroid control patients, whose TIC ranged from 2.5 to 14 mg, the TIC increased from 1.5 to 4 mg after 4 wk of treatment and had a tendency to plateau when the treatment was pursued. No significant changes in serum T4, T3, and TSH levels have been observed in these control subjects. Fourteen patients with autoimmune thyroiditis with low TIC (0-5 mg) were also studied. In six patients, the TIC increased significantly (3-10 mg over initial value after 3-7 mo of treatment). In parallel, there was a significant increase in serum T4 levels (35-150% over initial value) while T3 levels were modified in only two patients. In five patients serum TSH level decreased and was two- to seven-fold lower than before treatment whatever was its initial value; however, the spectrum of changes varied among patients from slight increase to a complete normalization of hormonosynthesis. In the eight other patients, iodide supplementation aggravated the thyroid disorders during the first months of treatment. The thyroid hormone blood levels dropped significantly in six patients (percent decrease below initial value: 20-100%) and was unchanged in the two others. An increase in the TSH blood level (X2-6) was observed in all patients except one. Concomitantly, the iodine stores were progressively depleted in three patients, unchanged in three and increased in two. When iodide treatment was pursued, an escape from this organification block was observed in two patients.

Adult↗
PubMed1988

Growth factors and the thyroid: effects of treatment for hyper- and hypothyroidism on serum IGF-I and urinary epidermal growth factor concentrations.

We investigated the impact of thyroid hormone levels on serum concentrations of IGF-I and urinary epidermal growth factor (EGF) in hyper- and hypothyroid patients before and during medical treatment. Serum IGF-I levels measured with radioreceptor-assay decreased in 12 hyperthyroid patients from 1.25 (1.02-1.80) to 1.02 (0.77-1.78) X 10(3) U/l (P less than 0.01), whereas a non-significant increase in 8 hypothyroid patients--from 1.14 (0.85-1.40) to 1.39 (1.08-1.80) X 10(3) U/l was recorded. Urinary EGF, measured with radioimmunoassay decreased in 10 hyperthyroid patients from 68.0 (38.0-122.9) to 40.9 (23.6-100.3) micrograms/g creatinine (P less than 0.001) and increased in 7 hypothyroid subjects from 23.8 (17.5-35.8) to 36.1 (24.7-60.1) micrograms/g creatinine (P less than 0.05). In hyperthyroidism, but not in hypothyroidism, the urinary excretion of creatinine changed significantly from 0.66 (0.26-1.21) to 1.52 (0.81-2.59) g/l (P less than 0.001) during treatment, thus affecting the EGF excretion values. However, a comparison of untreated hyperthyroid with untreated hypothyroid patients showed a highly significant difference in EGF excretion (P less than 0.001) despite a non-significant difference in creatinine excretion between the two groups. FT4 I concentrations correlated significantly (r = 0.83) (P less than 0.001) to EGF values in untreated hyper- and hypo-thyroid patients. Data from the present study thus conform with the view that the growth promoting effect of thyroid hormones involves a stimulated synthesis or release of classic growth factors.

Adult↗
PubMed1986

Autoantibodies to thyroid peroxidase in patients with chronic thyroiditis: effect of antibody binding on enzyme activities.

Using thyroid peroxidase (TPO), which was purified from the thyroid of patients with Graves' disease, we attempted to determine whether sera from patients with chronic thyroiditis contained antibodies to the enzyme. When the binding was tested by ELISA, sera from patients with chronic thyroiditis revealed high binding activities to TPO. When TPO was incubated with IgG from sera followed by treatment with protein A-Sepharose and centrifugation, the remaining TPO activities in the supernatant fraction were lower in most of the patients, as compared to normal controls. Moreover, IgG purified by DEAE-cellulose chromatography from sera in patients interfered with the TPO activities. Titres of anti-TPO antibodies correlated well with those of anti-microsome antibodies. These results indicate the presence of autoantibodies to TPO in sera of most patients with chronic thyroiditis and that TPO may be one component of microsome antigen complexes recognized by the autoantibodies. Studies on the inhibition of TPO by IgG isolated from sera of patients using guaiacol and iodide assays revealed that at least three epitopes of TPO molecule were recognized by autoantibodies and that the antigenic determinants on TPO molecule recognized by autoantibodies could be heterogeneous in patients.

Adolescent↗
PubMed1986

Reparative growth in the rat thyroid: effect of TSH suppression.

Previous investigations have shown that thyroid incision leads to a dramatic burst of follicular cell mitotic activity in cells adjacent to the wound edge in both normal rats and rats made hypothyroid by chronic goitrogen administration. Wound-induced thyroid mitotic activity therefore, is seen in rats with either normal or supranormal levels of circulating thyrotropin (TSH). This study was designed to investigate the thyroid mitotic response to wounding in the absence of detectable levels of circulating TSH. Rats were injected with large doses of L-thyroxine twice daily to render circulating TSH undetectable. Thyroids were incised and follicular cell mitotic activity, in relation to distance from the incision, determined at 24, 48 and 72 hr after incision. A mitotic response to wounding was maintained in L-thyroxine treated rats, even though circulating TSH was undetectable. The peak of activity was at 48 hr, but was only 50% of that found in the incised normal rat thyroid. The spatial distribution of the response suggests that there are two components of the wound response in the normal thyroid, one dependent on the presence of circulating TSH, the other TSH-independent. The results are discussed in relation to current understanding of cellular growth control.

Animals↗
PubMed1988

Role of calcium in the secretomotor response of the thyroid: effects of calcium ionophore A23187 on radioiodine turnover, membrane potential and fluid transport in cultured porcine thyroid cells.

The calcium ionophore A23187 (0.1-1 mumol/l) inhibited membrane electrical polarization, uptake of 125I, fluid transport and TSH-stimulated release of radioiodine from the organic pool in follicular cultures of porcine thyroid cells. At higher concentrations (1-30 mumol/l), A23187 promoted release of radioiodine from the organic pool. Stimulation of release of radioiodine from the organic pool by veratridine (a sodium channel agonist, 0.4-1 mmol/l) and A23187 was dependent on the calcium concentration of the medium, while TSH action was independent. Incubation in medium of very low calcium concentration (0.0177 mmol/l) resulted in enhanced release from the organic pool, which was inhibited by TSH (256 microU/ml), A23187 (25 mumol/l) or veratridine (0.5 mmol/l). These data therefore do not support the hypothesis that calcium acts as a mediator of the secretomotor action of TSH, but suggest the possibility of a TSH-induced increase in intracellular calcium as a regulatory negative-feedback mechanism.

Animals↗
PubMed1989

Pituitary-adrenal and thyroid effects on melatonin content of the rat pineal gland.

Based on clinical findings of diminished nocturnal serum melatonin levels in affective illness, we hypothesized that alterations in the pituitary-adrenal or thyroid axes of the rat might alter the nocturnal rise of melatonin content of the pineal gland in that species. Two experiments were conducted to investigate these issues. In the first, rats were injected for nine days with adrenocorticotropic hormone (ACTH) or corticosterone, timed to accentuate and prolong the normal circadian corticosterone rise. Although both these treatments produced significant elevations of serum corticosterone, there was no difference in pineal melatonin content during the day or night from that measured in control rats. In the second experiment, hypothyroidism was induced in rats by thyroid-parathyroidectomy, and hyperthyroidism was produced by injection of triiodothyronine (T3) for nine days. Despite clear evidence of metabolic and endocrine effects of these thyroid manipulations, pineal melatonin content was not altered during the day or night. The nocturnal increase of melatonin may have been phase-advanced in the hypothyroid group, although the experiment was not designed to detect such a shift. There thus is no evidence from this study in the rat to suggest that diminished nocturnal melatonin production in affective illness might be due to associated alterations in the pituitary-adrenal or thyroid systems.

Adrenocorticotropic Hormone↗
PubMed1986

[Crystalline inclusions of the mouse thyroid. Effect of chronic treatment with lithium gluconate].

Intracytoplasmic crystalline bodies of various sizes are found in thyroid cells of 10-month-old mice and in younger animals under chronic lithium treatment. They are frequently surrounded by small microvesicles and dense bodies or enclosed in larger vesicles having a dense content. The crystalline skeleton is a network of protein fibers assembled in a characteristic axis with a periodicity of 8 nm. A deficiency of thyroid cell metabolism related to aging or lithium gluconate treatment would lead to an accumulation of substances of a crystalline pattern.

Aging↗
PubMed1988

Pituitary-thyroid interaction: effects of thyroid hormone, non thyroidal illness and various agents on TSH secretion.

Recent developments in thyroid hormone metabolism have helped to understand the complex events which characterize the regulation of TSH secretion. Plasma T3 concentration as well as intrapituitary T3 generation from T4, exert a profound effect on TSH synthesis and release. Pituitary Type II deiodinase differs from Type I deiodinase found in other tissue such as liver and kidney, and in fact different conditions such as hypothyroidism and hyperthyroidism affect these enzymes in opposite direction. Thyroid hormones exert other effects on the pituitary such as increased synthesis of substance P, increased synthesis of GH, and decreased TRH receptors, TRH also modifies its own receptors in the pituitary and exerts modulatory effects on TSH molecule. Patients with non thyroidal illness may display TSH molecules with decreased biological activity. Various agents used in every day praxis may alter TSH and thyroid secretion. The physician must be aware of changes in order to avoid diagnostic pitfalls.

Animals↗
PubMed1987

Thyroid effects on adenosine 3',5'-monophosphate levels and adenylate cyclase in cultured neuroblastoma cells.

Using neuroblastoma cells as a model of developing neurons, we have tested the hypothesis that thyroid hormones alter cAMP metabolism. Neuroblastoma cells were grown in serum-free defined medium for 48 h with or without thyroid hormones. Treatment with 20-200 nM 3,5,3'-triiodo-L-thyronine (T3) increased the accumulation of cAMP by intact cells without altering growth, gross morphology, or DNA or protein content. The increase in cAMP accumulation could be detected 5 h after the addition of T3 and was abolished by the addition of cycloheximide. The maximum stimulation produced by prostaglandin E1 was increased in T3 cells without a significant alteration of the half-maximal concentration. T4 and D-T3 in concentrations up to 20 microM did not increase cAMP accumulation. Adenylate cyclase activity in response to forskolin, guanine nucleotides, and stimulatory hormones was increased in purified membranes from cells grown in T3, suggesting that increased adenylate cyclase is probably the major mechanism of the observed response to thyroid hormone.

Adenylyl Cyclases↗