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S Chan
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CJ McCabe
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TJ Visser
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JA Franklyn
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MD Kilby
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N-TERA-2 cl/D1 (NT2) cells, a human embryonal cell line with characteristics of central nervous system precursor cells, were utilised to study thyroid hormone action during early neuronal growth and differentiation. Undifferentiated NT2 cells expressed mRNAs encoding thyroid hormone receptors (TRs) alpha1, alpha2 and beta1, iodothyronine deiodinases types 2 (D2) and 3 (D3) (which act as the pre-receptor regulators), and the thyroid hormone-responsive genes myelin basic protein (MBP) and neuroendocrine specific protein A (NSP-A). When terminally differentiated into post-mitotic neurons (hNT), TRalpha1 and TRbeta1 mRNA expression was decreased by 74% (P=0.05) and 95% (P<0.0001) respectively, while NSP-A mRNA increased 7-fold (P<0.05). However, mRNAs encoding TRalpha2, D2, D3 and MBP did not alter significantly upon neuronal differentiation and neither did activities of D2 and D3. With increasing 3,5,3'-triiodothyronine (T(3)) concentrations, TRbeta1 mRNA expression in cultured NT2 cells increased 2-fold at 10 nM T(3) and 1.3-fold at 100 nM T(3) (P<0.05) compared with that in T(3)-free media but no change was seen with T(3) treatment of hNT cells. D3 mRNA expression in NT2 cells also increased 3-fold at 10 nM T(3) (P=0.01) and 2.4-fold at 100 nM T(3) (P<0.05) compared with control, but there was no change in D3 enzyme activity. In contrast there was a 20% reduction in D3 mRNA expression in hNT cells at 10 nM T(3) (P<0.05) compared with control, with accompanying reductions in D3 activity with increasing T(3) concentrations (P<0.05). There was no significant change in the expression of the TRalpha isoforms, D2, MBP and NSP-A with increasing T(3) concentrations in either NT2 or hNT cells. Undifferentiated NT2 and differentiated hNT cells show differing patterns of T(3)-responsiveness, suggesting that there are different regulatory factors operating within these cell types.

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OPHELIA GONA
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A. G. GONA
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Montclair State College, Department of Biology, Upper Montclair, New Jersey 07043, and *New Jersey Medical School, Newark, New Jersey 07103, U.S.A.

(Received 15 September 1975)

In recent years, there have been reports of an antagonistic effect between prolactin and thyroxine in amphibians (Bern, Nicoll & Strohman, 1967; Etkin & Gona, 1967; Gona, 1967) as well as in mammals (Mittra, 1974). In the red-spotted newt, Notophthalmus (Triturus) viridescens, we have been able to obtain the antagonistic effect described by Grant & Cooper (1965) with relatively large doses of thyroxine (Gona, Pearlman & Etkin, 1970). However, in hypophysectomized and thyroidectomized red efts (terrestrial stage of the red-spotted newt), the second metamorphosis-inducing effect of prolactin was greatly facilitated by 0·01 ng thyroxine/g body weight (Gona, Pearlman & Gona, 1973). In view of the report that the effect of prolactin on the mammary gland is most pronounced in the absence of thyroid hormone (Mittra,

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S Benvenuti
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P Luciani
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I Cellai
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C Deledda
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S Baglioni
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R Saccardi Endocrine Unit, Department of Haematology, Anatomy, Section of Endocrinology, Department of Clinical Physiopathology, Center for Research, Transfer and High Education on Chronic, Inflammatory, Degenerative and Neoplastic Disorders for the Development of Novel Therapies’ (DENOThe), University of Florence, Viale Pieraccini, 6, 50139 Florence, Italy

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S Urbani Endocrine Unit, Department of Haematology, Anatomy, Section of Endocrinology, Department of Clinical Physiopathology, Center for Research, Transfer and High Education on Chronic, Inflammatory, Degenerative and Neoplastic Disorders for the Development of Novel Therapies’ (DENOThe), University of Florence, Viale Pieraccini, 6, 50139 Florence, Italy

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F Francini Endocrine Unit, Department of Haematology, Anatomy, Section of Endocrinology, Department of Clinical Physiopathology, Center for Research, Transfer and High Education on Chronic, Inflammatory, Degenerative and Neoplastic Disorders for the Development of Novel Therapies’ (DENOThe), University of Florence, Viale Pieraccini, 6, 50139 Florence, Italy

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R Squecco Endocrine Unit, Department of Haematology, Anatomy, Section of Endocrinology, Department of Clinical Physiopathology, Center for Research, Transfer and High Education on Chronic, Inflammatory, Degenerative and Neoplastic Disorders for the Development of Novel Therapies’ (DENOThe), University of Florence, Viale Pieraccini, 6, 50139 Florence, Italy

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C Giuliani
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G B Vannelli Endocrine Unit, Department of Haematology, Anatomy, Section of Endocrinology, Department of Clinical Physiopathology, Center for Research, Transfer and High Education on Chronic, Inflammatory, Degenerative and Neoplastic Disorders for the Development of Novel Therapies’ (DENOThe), University of Florence, Viale Pieraccini, 6, 50139 Florence, Italy

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M Serio
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A Pinchera Endocrine Unit, Department of Haematology, Anatomy, Section of Endocrinology, Department of Clinical Physiopathology, Center for Research, Transfer and High Education on Chronic, Inflammatory, Degenerative and Neoplastic Disorders for the Development of Novel Therapies’ (DENOThe), University of Florence, Viale Pieraccini, 6, 50139 Florence, Italy

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A Peri
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Introduction Thyroid hormones (TH) play a fundamental role in fetal life, particularly in promoting brain development. TH affect the expression of several genes, which are related to cell migration (i.e. reelin, laminin, tenascin C), myelination (i

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CH Kim
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HK Kim
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YK Shong
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KU Lee
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GS Kim
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It is well known that excessive thyroid hormone in the body is associated with bone loss. However, the mechanism by which thyroid hormone affects bone turnover remains unclear. It has been shown that it stimulates osteoclastic bone resorption indirectly via unknown mediators secreted by osteoblasts. To determine if interleukin-6 (IL-6) or interleukin-11 (IL-11) could be the mediator(s) of thyroid hormone-induced bone loss, we studied the effects of 3,5,3'-tri-iodothyronine (T3) on basal and interleukin-1 (IL-1)-stimulated IL-6/IL-11 production in primary cultured human bone marrow stromal cells. T3 at 10(-12)-10(-8) M concentration significantly increased basal IL-6 production in a dose-dependent manner. It also had an additive effect on IL-1-stimulated IL-6 production, but failed to elicit a detectable effect on basal or IL-1-stimulated IL-11 production. Treatment with 17beta-estradiol (10(-8) M) did not affect the action of T3 on IL-6/IL-11 production. These results suggest that thyroid hormone may stimulate bone resorption by increasing basal and IL-1-induced IL-6 production from osteoblast-lineage cells, and these effects are independent of estrogen status.

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Alison Mostyn Institute of Clinical Research, Centre for Reproduction and Early Life, University Hospital, Nottingham NG7 2UH, UK
Department of Agricultural Sciences, Imperial College London, Wye Campus, Ashford, Kent TN25 5AH, UK

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Sylvain Sebert Institute of Clinical Research, Centre for Reproduction and Early Life, University Hospital, Nottingham NG7 2UH, UK
Department of Agricultural Sciences, Imperial College London, Wye Campus, Ashford, Kent TN25 5AH, UK

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Jennie C Litten Institute of Clinical Research, Centre for Reproduction and Early Life, University Hospital, Nottingham NG7 2UH, UK
Department of Agricultural Sciences, Imperial College London, Wye Campus, Ashford, Kent TN25 5AH, UK

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Katharine S Perkins Institute of Clinical Research, Centre for Reproduction and Early Life, University Hospital, Nottingham NG7 2UH, UK
Department of Agricultural Sciences, Imperial College London, Wye Campus, Ashford, Kent TN25 5AH, UK

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John Laws Institute of Clinical Research, Centre for Reproduction and Early Life, University Hospital, Nottingham NG7 2UH, UK
Department of Agricultural Sciences, Imperial College London, Wye Campus, Ashford, Kent TN25 5AH, UK

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Michael E Symonds Institute of Clinical Research, Centre for Reproduction and Early Life, University Hospital, Nottingham NG7 2UH, UK
Department of Agricultural Sciences, Imperial College London, Wye Campus, Ashford, Kent TN25 5AH, UK

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Lynne Clarke Institute of Clinical Research, Centre for Reproduction and Early Life, University Hospital, Nottingham NG7 2UH, UK
Department of Agricultural Sciences, Imperial College London, Wye Campus, Ashford, Kent TN25 5AH, UK

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piglet physiology between the two breeds. Thyroxine (T 4 ) and T 3 are both present in colostrum and milk at concentrations that vary between species ( Akasha & Anderson 1984 ). Thyroid hormones regulate energy metabolism by increasing respiration and

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E. NIESCHLAG
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J. HERRMANN
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K. H. USADEL
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U. SCHWEDES
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K. SCHÖFFLING
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H. L. KRÜSKEMPER
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According to the concept of negative feedback control, thyroid hormones act on hypothalamo-pituitary receptors to reduce further secretion of thyroid-stimulating hormone (TSH). Only the free non-protein-bound fraction of circulating thyroid hormone appears to be biologically active and available to the central receptors (Robbins & Rail, 1967). Antibodies to thyroid hormones introduced into the circulation by active immunization should reduce the biologically active hormone fraction and thus cause increased TSH secretion followed by characteristic morphological and functional changes.

In order to test the validity of this concept, 12-week-old, male, New Zealand White rabbits were immunized with L-tri-iodothyronine (T3) or L-thyroxine (T4) conjugates (Oliver, Parker, Brasfield & Parker, 1968) following the method of Vaitukaitis, Robbins, Nieschlag & Ross (1971). The thyroid glands of one animal immunized with T3 and of one immunized with T4 and of three control animals of the same age and sex were

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P. G. Newrick
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G. Braatvedt
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D. Stansbie
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R. J. M. Corrall
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ABSTRACT

To determine whether increases in non-esterified fatty acids alter free thyroid hormone and TSH levels, the effect of endogenous activation of lipolysis by insulin-induced hypoglycaemia was examined in seven healthy volunteers pretreated with placebo or acipimox. Whilst levels of non-esterified fatty acid were very different in the two groups, levels of free thyroxine, tri-iodothyronine and TSH were unchanged. Thus, within the range of non-esterified fatty acid levels likely to be seen in clinical practice, any effect on thyroid hormone measurements can be safely ignored.

Journal of Endocrinology (1991) 130, 155–157

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A. ŚLEBODZIŃSKI
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SUMMARY

1. The effect of 250 μg./day stilboestrol on thyroid hormone metabolism in sheep has been investigated.

2. After 5 days the conversion ratio was significantly increased and the rate of release of iodine from the thyroid also rose.

3. After 40 days the thyroxine utilization rate increased but the turnover rate was reduced. This effect was presumably due to a coincident increase in the plasma protein-bound iodine and the thyroxine distribution space.

4. It is suggested that small doses of oestrogen decrease tissue metabolism, inducing increased activity of the thyroid gland and a compensatory increase in the peripheral utilization of thyroid hormone.

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T. J. Lauterio
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C. G. Scanes
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ABSTRACT

The possible role of thyroid hormones in the rise in plasma GH observed in protein-restricted chicks was examined. Increased sensitivity of protein-restricted chicks to secretagogue challenge (TRH or GH-releasing factor) appears to account, at least in part, for increased GH concentrations in protein-restricted chicks. Thyroid hormones administered acutely were able to suppress plasma GH concentrations in protein-restricted chicks. Further, chronic thyroid hormone supplementation to low protein diets normalized circulating thyroid hormone concentrations and also normalized the response to GH secretagogue challenge. This decreased sensitivity to TRH provocation occurred without an accompanying change in plasma concentrations of insulin-like growth factor-I, a reputed inhibitor of GH secretion in the chicken.

J. Endocr. (1988) 117, 223–228

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A. W. G. GOOLDEN
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JUNE M. GARTSIDE
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C. OSORIO
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SUMMARY

Blood samples obtained from normal people after an oral dose of 0·4 mg. l-thyroxine showed a depression in the uptake of [131I]tri-iodothyronine ([131I]T3) by the red cells, whereas the uptake by a resin sponge was increased. This depression did not occur when the test was carried out at 20° instead of at 37°. It was reversed when methylthiouracil, which is known to inhibit deiodination, was added to the blood in vitro. These findings are indicative of deiodination as the cause of the depression of T3-red cell (RBC) uptake. T3-RBC uptake was similarly depressed after the administration of l-tri-iodothyronine, and it was concluded that deiodination was promoted in the red cell system whenever there was an increase in the level of circulating thyroid hormone.

The radioactive product of deiodination, which may be an artifact rather than a natural metabolite, has not been identified. Analysis of plasma obtained from blood after incubation with [131I]T3 under the conditions of the T3-RBC test, has not shown any [131I]iodide other than that present as an impurity in the [131I]T3 preparation. It could be shown that the product of deiodination is bound by the red cells but is eluted from them more readily than [131I]T3. It is suggested that the fall in T3-RBC uptake after thyroxine is due to deiodination which results in the formation of some radioactive product which is eluted from the red cells in the washing procedure.

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