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  • Abstract: Thyroid* x
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R. S. Sundick, D. Herdegen, T. R. Brown, A. Dhar and N. Bagchi

ABSTRACT

Several studies have shown that iodine plays a role in spontaneous autoimmune thyroiditis in man and other animals. In addition, abnormalities of iodine metabolism have been found in patients with Hashimoto's thyroiditis and in chickens of the obese strain (OS), an animal model of spontaneous autoimmune thyroiditis. We have examined several parameters of iodine metabolism before immune damage in this model and in the related Cornell strain (CS), a strain which develops a late-onset mild thyroiditis, to discover a possible causal relationship between altered iodine metabolism and the initiation of autoimmunity.

Thyroglobulin was purified from individual chicken thyroid glands and analysed for iodine by the ceric sulphate method. Analogous to the thyroglobulin of Hashimoto's patients, the iodine content of OS thyroglobulin (27 atoms/molecule) was lower than that of normal-strain thyroglobulin (46 atoms/molecule) when the chickens were provided with a normal diet. Also, under conditions of TSH suppression, the iodine content of OS thyroglobulin (18 atoms/molecule) was lower than that of CS thyroglobulin (36 atoms/molecule) and of normal-strain thyroglobulin (32 atoms/molecule). In contrast with Hashimoto's patients, however, the OS and CS chickens had practically no inorganic iodide in their thyroid glands; electrophoretic analysis of thyroid homogenates revealed that essentially all (> 99·62%) 125I was organified by 16 h in all strains of birds tested. Despite the relatively poor iodination of thyroglobulin exhibited by OS chickens, they did not iodinate additional 'unique' proteins, when examined by sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) of thyroid proteins labelled with 125I in vivo.

The release of 125I in vivo under conditions of TSH suppression was examined in chicks receiving thyroxine and propylthiouracil. After 14 days both OS and CS chicks showed poorly suppressible release of 85% and 92% respectively, while the normal strain released 33 %. To determine whether the autonomous function of OS and CS thyroid glands was present in a restricted number of follicles or cells or whether it occurred in a majority of cells, autoradiograms of thyroid glands labelled in vivo from TSH-suppressed chickens were examined. Silver grains were present in all cells, indicating that autonomous function was a characteristic of all cells.

These thyroid gland abnormalities are compared with those found in Hashimoto's patients and discussed in the context of their aetiological significance.

Journal of Endocrinology (1991) 128, 239–244

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M Makino, N Oda, N Miura, S Imamura, K Yamamoto, T Kato, K Fujiwara, Y Sawai, K Iwase, A Nagasaka and M Itoh

Thyroid hormones affect reactions in almost all pathways of lipid metabolism. It has been reported that plasma free fatty acid (FFA) concentration in hypothyroidism is generally within the normal range. In this study, however, we show that plasma FFA concentration in some hypothyroid patients is higher than the normal range. Symptoms of thyroid dysfunction in these individuals were less severe than those of patients with lower plasma FFA concentrations. From these findings we hypothesized that the change in FFA concentration must correlate with thyroid function. Using an animal model, we then examined the effect of highly purified eicosapentaenoic acid ethyl ester (EPA-E), a n-3 polyunsaturated fatty acid derived from fish oil, on thyroid function in 1-methyl-2-imidazolethiol (MMI)-induced hypothyroid rats. Oral administration of EPA-E inhibited reduction of thyroid hormone levels and the change of thyroid follicles in MMI-induced hypothyroid rats. These findings suggest that FFA may affect thyroid functions and EPA-E may prevent MMI-induced hypothyroidism.

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J. P. THAPLIYAL, ASHA CHANDOLA, D. SURESH KUMAR and O. V. OOMMEN

Department of Zoology, Banaras Hindu University, Varanasi 221005, India

(Received 18 June 1974)

Male hormone has been classically attributed a primary role in the maintenance of reproductive function in male vertebrates. Thyroid hormone on the other hand has been shown to control oxidative metabolism in homeotherms, but its role in poikilothermous animals has not been established, except in reptiles (see reviews by Dodd & Matty, 1964; Lynn, 1970). Recently oxidative metabolism was shown to be influenced by testosterone in three species of reptiles, namely, Calotes versicolor (Chandola, Kumar & Thapliyal, 1974a), Natrix piscator (Thapliyal, Kumar & Garg, 1974) and Hemidactylus flaviviridis (Chandola et al. 1974b). Castration in all these species resulted in a significant decrease and administration of testosterone in a significant increase in the oxygen consumption of isolated liver and skeletal muscle tissues (at 30 °C). Testosterone also restored the decline in oxygen consumption in castrated animals to normal

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M. C. THORNDYKE

In vertebrates, thyroid hormones exert multiple biological actions, one of the most thoroughly investigated effects being that concerned with protein synthesis. One of the more elegant experimental systems used in studies of this phenomenon, is the precocious induction of metamorphosis in amphibian tadpoles, by administration of thyroid hormones. Experiments by Tata (1969) and others, have demonstrated a marked increase in the synthesis of various enzymes involved in growth and metabolism during metamorphosis.

It has been shown on several occasions that ascidians are capable of producing limited quantities of thyroid hormones (Salvatore, Vecchio & Maccia, 1960; Roche, Salvatore & Rametta, 1962; Barrington & Thorpe, 1965; Salvatore, 1969). However, at present there is no evidence as to the possible role of these compounds in acidian growth and metabolism. Indeed, it is also open to question whether or not thyroid hormones exert any normal physiological role in non-vertebrates in general.

In the present

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J. S. JENKINS

SUMMARY

The extra-hepatic metabolism of cortisol in man has been studied in vitro by incubation of [4-14C]cortisol with tissue slices.

Kidney tissue was the most active, followed by prostate; thyroid, skeletal muscle and synovial membrane were much less effective. Cortisone was quantitatively the predominant metabolite but C-20-reduced derivatives of cortisol and cortisone were also present. There was evidence for the oxidation of the side chain by kidney and prostate, but no ring A-reduced compounds were found.

Kidney slices did not reduce the 11-oxo group of cortisone but this reaction proceeded readily with liver slices.

Some evidence for extra-hepatic metabolism of cortisol in vivo by the tissues of the forearm was obtained by infusing [4-14C]cortisol into the brachial artery.

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Stefan Groeneweg, Robin P Peeters, Theo J Visser and W Edward Visser

Thyroid hormone (TH) is crucial for development and metabolism of many tissues. The physiological relevance and therapeutic potential of TH analogs have gained attention in the field for many years. In particular, the relevance and use of 3,3′,5-triiodothyroacetic acid (Triac, TA3) has been explored over the last decades. Although TA3 closely resembles the bioactive hormone T3, differences in transmembrane transport and receptor isoform-specific transcriptional activation potency exist. For these reasons, the application of TA3 as a treatment for resistance to TH (RTH) syndromes, especially MCT8 deficiency, is topic of ongoing research. This review is a summary of all currently available literature about the formation, metabolism, action and therapeutic applications of TA3.

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Flavia F Bloise, Aline Cordeiro and Tania Maria Ortiga-Carvalho

Thyroid hormones (TH) are crucial for development, growth, differentiation, metabolism and thermogenesis. Skeletal muscle (SM) contractile function, myogenesis and bioenergetic metabolism are influenced by TH. These effects depend on the presence of the TH transporters MCT8 and MCT10 in the plasma membrane, the expression of TH receptors (THRA or THRB) and hormone availability, which is determined either by the activation of thyroxine (T4) into triiodothyronine (T3) by type 2 iodothyronine deiodinases (D2) or by the inactivation of T4 into reverse T3 by deiodinases type 3 (D3). SM relaxation and contraction rates depend on T3 regulation of myosin expression and energy supplied by substrate oxidation in the mitochondria. The balance between D2 and D3 expression determines TH intracellular levels and thus influences the proliferation and differentiation of satellite cells, indicating an important role of TH in muscle repair and myogenesis. During critical illness, changes in TH levels and in THR and deiodinase expression negatively affect SM function and repair. This review will discuss the influence of TH action on SM contraction, bioenergetics metabolism, myogenesis and repair in health and illness conditions.

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I. Gause and S. Edén

ABSTRACT

The hormonal regulation of GH binding and the effects of GH on glucose metabolism were studied in hypophysectomized rats. Male rats (130–140 g) were hypophysectomized and on the day after the operation treatment with one or a combination of two hormones was started and continued for 7 days. The different hormonal treatments were (1) cortisone acetate, (2) insulin, (3) insulin plus cortisone acetate, (4) thyroxine, (5) thyroxine plus cortisone acetate and (6) GH. Glucose metabolism was studied by determining the production of CO2 from [14C]glucose in epididymal fat pads and adipocytes and the incorporation of [14C]glucose into lipids in adipocytes. Binding of GH was measured in cell aliquots using 125I-labelled human GH.

In hypophysectomized control animals, GH binding was decreased to approximately 25% of the binding observed in adipocytes of normal rats. Insulin treatment increased GH binding by approximately 100% and the response to GH was markedly increased. Similar effects were achieved by thyroxine treatment. Basal levels of glucose oxidation were markedly decreased after hypophysectomy but were increased towards normal by insulin or thyroxine treatment. Neither cortisone nor GH treatment had any effect on GH binding or glucose metabolism.

The results show that insulin and thyroxine may be important for the GH receptor and the insulin-like effect of GH in adipocytes.

J. Endocr. (1985) 105, 331–337

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S. PAPADOPOULOS, S. MacFARLANE and R. McG. HARDEN

SUMMARY

The relative affinities of the thyroid gland for 131I and 99mTcO4 and the further metabolism of these isotopes were studied in rats. 99mTcO4 is trapped to an extent almost identical to 131I in the thyroid. This process is inhibited by KClO4 and stimulated by thyroid-stimulating hormone. 99mTcO4 having been trapped is further metabolized in the thyroid gland.

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R. L. SUTHERLAND and M. W. SIMPSON-MORGAN

The concentration of circulating plasma thyroxine (T4) appears to have little effect on the maximal binding capacity of plasma thyroxine-binding globulin (TBG). Several studies in man have shown that thyrotoxicosis results in normal or slightly lowered levels of TBG, while hypothyroidism leads to a normal or slightly increased TBG binding capacity (Oppenheimer, Squef, Surks & Hauer, 1963; Inada & Sterling, 1967; Gordon, Kleinerman, Ehrenfeld & Ehrenfeld, 1971). In contrast the binding capacities of corticosteroid-binding globulin (CBG) and sex steroid-binding globulin (SBG) have been shown to be markedly affected by the level of circulating thyroid hormone. In the rat the binding capacity of CBG was markedly depressed by thyroid-ectomy and enhanced by chronic administration of T4 (Labrie, Raynaud & Fortier, 1965). Similarly, Dray, Mowszowicz, Ledru, Crépy, Delzant & Sebaoun (1969) administered T4 to normal human subjects and observed an increase of SBG concentration. Hyperthyroidism has been shown to