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T Mano, R Sinohara, Y Sawai, N Oda, Y Nishida, T Mokuno, M Kotake, M Hamada, R Masunaga, A Nakai and A Nagasaka

Abstract

Active oxygen species are reported to cause organ damage. This study was therefore designed to determine the behaviour of antioxidants and free radical scavengers so as to reveal changes in animals in the hyper- and hypothyroid state.

Levels of antioxidant factors (i.e. coenzyme Q (CoQ)10, CoQ9 and vitamin E) and free radical scavengers (catalase, glutathione peroxidase (GSH-PX) and superoxide dismutase (SOD)) were measured in the heart muscles of rats rendered hyper- or hypothyroid by 4 weeks of thyroxine (T4) or methimazol treatment. Serum levels of CoQ9 and total SOD were also measured.

A significant reduction in CoQ9 levels was observed in the heart muscles of both hyper- and hypothyroid rats when compared with control hearts. There was no difference in serum CoQ9 levels in thyroid dysfunction when compared with control animals. Levels of vitamin E in the heart muscles of hyperthyroid rats were significantly increased, and there was no reduction in vitamin E levels in hypothyroid rats when compared with control hearts. GSH-PX levels in the heart muscle were reduced in hyperthyroid rats and increased in hypothyroid rats when compared with control hearts. However, there were no differences in catalase levels in heart muscle between hyper- and hypothyroid rats. The concentration of SOD in heart muscle was increased in hyperthyroid rats and was not decreased in hypothyroid rats compared with control rats, suggesting the induction of SOD by excessive production of O2 .

These data suggest that the changes in these scavengers have some role in cardiac dysfunction in the hyper- and hypothyroid state in the rat.

Journal of Endocrinology (1995) 145, 131–136

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A. ŚLEBODZIŃSKI

SUMMARY

(1) The interaction between thyroid hormone and thyroxine-binding globulin (TBG) has been studied in 39 pigs from eight litters, aged from 12 hr. to 11 days. In addition, single observations were made on six batches of 42 pigs from 1 day to 6 months old and in five newborn sheep.

(2) A rapid increase in the level of the unsaturated TBG capacity was found to occur from the 1st day after birth.

(3) Continuous changes in the unsaturated TBG capacity resulted in a decline in the plasma level of free thyroxine and in a decrease in the uptake of [131I]triiodothyronine by erythrocytes. Equilibrium between the hormonal iodine metabolism and its blood carrier is reached at the end of the 1st week of life.

(4) These findings suggest that in discussing thyroid metabolism in neonatal animals it is important to distinguish between the early neonatal adaptive period and the remainder of the period of thyroid hyperactivity. The physiological implications of the higher level of free thyroxine in the blood after birth for the adaptation to post-uterine life is discussed.

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SM van der Heide, TJ Visser, ME Everts and PH Klaren

We have investigated the potential role of fibroblasts in local thyroid hormone metabolism in neonatal rat heart. Incubation of cardiac fibroblasts with thyroxine (T4) or 3,5,3'-tri-iodothyronine (T3) resulted in the appearance of water-soluble metabolites, whereas incubation of cardiomyocytes under the same conditions did not or did so to a much lesser extent. Time-course studies showed that production is already evident after 1-5 h of exposure and that the process equilibrates after 24-48 h. Analysis of the products revealed both the T4 and the T3 metabolites to be glucuronides. These results were corroborated by the detection of uridine diphosphate (UDP)-glucuronyltransferase activity in cardiac fibroblasts. We found no indication for outer ring deiodination in fibroblasts, cardiomyocytes or heart homogenates. From these results we have concluded that cardiac fibroblasts, but not cardiomyocytes, are able to glucuronidate T4 and T3 and secrete the conjugates. This could play a role in local metabolism, e.g. to protect the heart tissue from high levels of thyroid hormones.

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J Patel, K Landers, H Li, R H Mortimer and K Richard

The development of fetal thyroid function is dependent on the embryogenesis, differentiation, and maturation of the thyroid gland. This is coupled with evolution of the hypothalamic–pituitary–thyroid axis and thyroid hormone metabolism, resulting in the regulation of thyroid hormone action, production, and secretion. Throughout gestation there is a steady supply of maternal thyroxine (T4) which has been observed in embryonic circulation as early as 4 weeks post-implantation. This is essential for normal early fetal neurogenesis. Triiodothyronine concentrations remain very low during gestation due to metabolism via placental and fetal deiodinase type 3. T4 concentrations are highly regulated to maintain low concentrations, essential for protecting the fetus and reaching key neurological sites such as the cerebral cortex at specific developmental stages. There are many known cell membrane thyroid hormone transporters in fetal brain that play an essential role in regulating thyroid hormone concentrations in key structures. They also provide the route for intracellular thyroid hormone interaction with associated thyroid hormone receptors, which activate their action. There is a growing body of experimental evidence from rats and humans to suggest that even mild maternal hypothyroxinemia may lead to abnormalities in fetal neurological development. Our review will focus on the ontogeny of thyroid hormone in fetal development, with a focus on cell membrane transporters and TR action in the brain.

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L. F. B. P. Costa Rosa, Y. Cury and R. Curi

ABSTRACT

In the present study the effects of insulin, glucocorticoids and thyroid hormones on macrophage metabolism and function were investigated. The maximum activities of hexokinase, glucose-6-phosphate dehydrogenase, glutaminase and citrate synthase were determined in macrophages obtained from hormonetreated rats and those cultured for a period of 48 h in the presence of hormones. Macrophage phagocytosis was markedly inhibited by dexamethasone and thyroid hormones, remaining unchanged when insulin was added to the culture medium, however. The changes in the enzyme activities caused by hormone treatments of the rats were very similar to those found in culture. Insulin enhanced citrate synthase and hexokinase activities and diminished those of glutaminase and glucose-6-phosphate dehydrogenase. Dexamethasone had a similar effect except on glucose6-phosphate dehydrogenase. The addition of thyroid hormones to the culture medium raised the activities of glutaminase and hexokinase and reduced that of citrate synthase. The results presented support the suggestion that the effects of insulin, glucocorticoids and thyroid hormones on immune and inflammatory responses could well be mediated through changes in macrophage metabolism..

Journal of Endocrinology (1992) 135, 213–219

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Anita Boelen, Anne H van der Spek, Flavia Bloise, Emmely M de Vries, Olga V Surovtseva, Mieke van Beeren, Mariette T Ackermans, Joan Kwakkel and Eric Fliers

Illness induces major modifications in central and peripheral thyroid hormone (TH) metabolism, so-called nonthyroidal illness syndrome (NTIS). As a result, organ-specific changes in local TH availability occur depending on the type and severity of illness. Local TH availability is of importance for the regulation of the tissue-specific TH target genes and determined by the interplay between deiodinating enzymes, TH transport and TH receptor (TR) expression. In the present study, we evaluated changes in TH transport, deiodination and TR expression, the resulting tissue TH concentrations and the expression of TH target genes in liver and muscle in three animal models of illness. We induced (1) acute systemic inflammation by intraperitoneal injection of bacterial endotoxin (LPS), (2) chronic local inflammation by a turpentine injection in the hind limb and (3) severe pneumonia and sepsis by intranasal inoculation with Streptococcus pneumoniae. We found that all aspects of peripheral TH metabolism are differentially regulated during illness, depending on the organ studied and severity of illness. In addition, tissue TH concentrations are not equally affected by the decrease in serum TH concentrations. For example, the decrease in muscle TH concentrations is less severe than the decrease observed in liver. In addition, despite lower TH concentrations in muscle in all three models, muscle T3 action is differentially affected. These observations help to understand the complex nature of the nonthyroidal illness syndrome.

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G. C. LIGGINS and P. C. KENNEDY

SUMMARY

Electrocoagulation lesions involving 70–100% of the hypophysis of 17 foetal lambs were made at various times between 93 and 136 days of gestation. Foetal growth and development after the operation was compared with that in a group of seven control lambs comprising three intact littermates of operated foetuses and four sham-operated foetuses. Hypophysial damage was found to be associated with retardation of somatic development which was most marked when the operation was performed early in gestation. Retardation was particularly evident in epiphysial development. Hypoplasia of the adrenal cortices, the interstitial cells of the testis and the thyroid glands confirmed the assumption made by previous workers based on decapitation experiments, that the foetal hypophysis exerts a trophic influence on the development of these endocrine organs. Reduced liver glycogen content and plasma glucose levels indicated a disturbed carbohydrate metabolism. Abnormal subcutaneous fat deposition suggested disorders in fat metabolism. Delayed involution of haemopoietic tissues, hypoplasia of peripheral lymphoid tissue and reduction in the number of mast cells in the skin were also noted. Structures of ectodermal origin were relatively unaffected by hypophysial lesions. It is concluded that the hypophysis of the foetal lamb subserves many of the functions attributed to it during extrauterine life.

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W. C. ADAMS and J. H. LEATHEM

SUMMARY

Immature female rats were fed thiouracil for 30 days and injected with 10 i.u. human chorionic gonadotrophin (HCG) for the last 20 days. In thiouracil-fed animals, HCG produced large ovaries containing follicular cysts. These ovaries showed a subnormal concentration of cholesterol but both a normal total content and normal incorporation of [1-14C]acetate into digitonin-precipitable-sterols. Liver and serum cholesterol concentrations were reduced, but in vivo, 4 hr. incorporation of acetate into sterols was doubled suggesting either an acceleration of cholesterol turnover or delayed utilization of sterol precursors of cholesterol. HCG also reduced ovarian cholesterol concentration in euthyroid animals but total organ content and incorporation of [14C]acetate were not altered, nor were liver and serum cholesterol affected. Since the effect of induced ovarian cysts on sterol metabolism cannot be accounted for by known effects of thyroid or gonadal hormones it is suggested that influences of steroid hormones on lipid metabolism may be greatly modified in thyroid deficiency.

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B. F. CLARK

Department of Hormone Physiology, Imperial Cancer Research Fund, Lincoln's Inn Fields, London, WC2A 3PX

(Received 19 February 1975)

Oestrogen treatment in vivo increases the metabolism of progesterone by the rat uterus in vitro (Armstrong & King, 1971; Howard & Wiest, 1972). However, the pattern of metabolites produced is dependent on the concentration of progesterone used in vitro (Saffron, Loeser, Haas & Stavely, 1974). When high concentrations of progesterone were used, oestrogen increased both ring A and C20-ketone metabolism. At low concentrations oestrogen increased C20-ketone metabolism, whereas ring A metabolism was decreased.

This present experiment was carried out to see whether oestrogen affected uterine metabolism of progesterone in vivo in mice (Clark, 1973, 1974) in the same way.

[1,2,6,7-3H] Progesterone (5 or 500 pg; sp. act. 261 μCi/μg, Radiochemical Centie, Amersham) was injected intraluminally into both uterine horns of spayed mice 1 or 6 days after oestrogen priming as described by

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A. Klein, A. W.-L. Chan and A. Malkin

ABSTRACT

Mononuclear cell preparations are capable of metabolizing cortisol to three metabolites which lack the immunosuppressive effect of their precursor. In the present study we noted a linear correlation, up to a point, between glucose concentration and the rate of human mononuclear cell cortisol metabolism in vitro. The mechanism by which glucose exerts its effect was investigated further. We observed that: (1) the effect of glucose on mononuclear cell cortisol metabolism was not influenced by insulin; (2) NADPH and NADH enhanced cortisol metabolism by disrupted cells, irrespective of whether the homogenates were dialysed or not; (3) lactate and ATP inhibited mononuclear cell cortisol metabolism and (4) almost all the glucose used was converted to lactate. It is concluded that mononuclear cell cortisol metabolism can depend on both nucleotides.

J. Endocr. (1986) 109, 181–185