Thyroid hormones and the mechanisms of adaptation to cold

HORMONES ◽  
2020 ◽  
Vol 19 (3) ◽  
pp. 329-339
Author(s):  
Sergey Tsibulnikov ◽  
Leonid Maslov ◽  
Nikita Voronkov ◽  
Peter Oeltgen
1981 ◽  
Vol 91 (3) ◽  
pp. 515-524 ◽  
Author(s):  
GERARD MORY ◽  
DANIEL RICQUIER ◽  
PIERRE PESQUIÉS ◽  
PHILIPPE HÉMON

Hypothyroidism was induced in adult rats by oral absorption of methimazole and its effects on brown adipose tissue (BAT) were studied. Hypothyroidism partially mimicked the effects of chronic exposure to cold: BAT weight and its DNA content were increased and the mitochondrial components (proteins, phospholipids) of the tissue were greatly enhanced when expressed per unit of fresh tissue weight. Moreover, hypothyroidism had the same effects as adaptation to cold on the fatty-acid composition of both total and mitochondrial phospholipids. Basal respiratory rate and total cytochrome C oxidase activity of the tissue were also increased. However, the increase in the concentration of the '32 000 mol. wt protein', a polypeptide which regulates the dissipation of heat by BAT, was smaller and non-selective in hypothyroid rats. The amount of this protein was increased per mg tissue, but not per mg mitochondrial proteins, as in rats adapted to cold. Furthermore, in contrast with the large mobilization of the lipid stores in BAT of euthyroid animals, the BAT lipid stores of hypothyroid rats were not mobilized during the first hours of exposure to cold. It may be concluded that (a) hypothyroidism induces several alterations in BAT which are characteristic of an active thermogenic state (this may be because of the response of the organism to the deficiency of thermogenesis induced by hypothyroidism), (b) this potential increase in thermogenic capacity in the BAT of hypothyroid rats has probably a limited physiological role, since thyroid hormones are necessary for the mobilization of the tissue lipids which are the fuel for production of heat and (c) these data provide evidence for a limited role of thyroid hormones in the trophic response of BAT during adaptation to cold.


2006 ◽  
Vol 5 (1) ◽  
pp. 56-56
Author(s):  
A BARISON ◽  
L RONDININI ◽  
S GUIDERI ◽  
M COCEANI ◽  
M SCARLATTINI ◽  
...  

2019 ◽  
Vol 89 (1-2) ◽  
pp. 80-88 ◽  
Author(s):  
Juliana Soares Severo ◽  
Jennifer Beatriz Silva Morais ◽  
Taynáh Emannuelle Coelho de Freitas ◽  
Ana Letícia Pereira Andrade ◽  
Mayara Monte Feitosa ◽  
...  

Abstract. Thyroid hormones play an important role in body homeostasis by facilitating metabolism of lipids and glucose, regulating metabolic adaptations, responding to changes in energy intake, and controlling thermogenesis. Proper metabolism and action of these hormones requires the participation of various nutrients. Among them is zinc, whose interaction with thyroid hormones is complex. It is known to regulate both the synthesis and mechanism of action of these hormones. In the present review, we aim to shed light on the regulatory effects of zinc on thyroid hormones. Scientific evidence shows that zinc plays a key role in the metabolism of thyroid hormones, specifically by regulating deiodinases enzymes activity, thyrotropin releasing hormone (TRH) and thyroid stimulating hormone (TSH) synthesis, as well as by modulating the structures of essential transcription factors involved in the synthesis of thyroid hormones. Serum concentrations of zinc also appear to influence the levels of serum T3, T4 and TSH. In addition, studies have shown that Zinc transporters (ZnTs) are present in the hypothalamus, pituitary and thyroid, but their functions remain unknown. Therefore, it is important to further investigate the roles of zinc in regulation of thyroid hormones metabolism, and their importance in the treatment of several diseases associated with thyroid gland dysfunction.


2019 ◽  
Vol 89 (1-2) ◽  
pp. 45-54
Author(s):  
Akemi Suzuki ◽  
André Manoel Correia-Santos ◽  
Gabriela Câmara Vicente ◽  
Luiz Guillermo Coca Velarde ◽  
Gilson Teles Boaventura

Abstract. Objective: This study aimed to evaluate the effect of maternal consumption of flaxseed flour and oil on serum concentrations of glucose, insulin, and thyroid hormones of the adult female offspring of diabetic rats. Methods: Wistar rats were induced to diabetes by a high-fat diet (60%) and streptozotocin (35 mg/kg). Rats were mated and once pregnancy was confirmed, were divided into the following groups: Control Group (CG): casein-based diet; High-fat Group (HG): high-fat diet (49%); High-fat Flaxseed Group (HFG): high-fat diet supplemented with 25% flaxseed flour; High-fat Flaxseed Oil group (HOG): high-fat diet, where soya oil was replaced with flaxseed oil. After weaning, female pups (n = 6) from each group were separated, received a commercial rat diet and were sacrificed after 180 days. Serum insulin concentrations were determined by ELISA, the levels of triiodothyronine (T3), thyroxine (T4) and thyroid-stimulating hormone (TSH) were determined by chemiluminescence. Results: There was a significant reduction in body weight at weaning in HG (−31%), HFG (−33%) and HOG (44%) compared to CG (p = 0.002), which became similar by the end of 180 days. Blood glucose levels were reduced in HFG (−10%, p = 0.044) when compared to CG, and there was no significant difference between groups in relation to insulin, T3, T4, and TSH after 180 days. Conclusions: Maternal severe hyperglycemia during pregnancy and lactation resulted in a microsomal offspring. Maternal consumption of flaxseed reduces blood glucose levels in adult offspring without significant effects on insulin levels and thyroid hormones.


1990 ◽  
Vol 29 (01) ◽  
pp. 40-43 ◽  
Author(s):  
W. Langsteger ◽  
P. Költringer ◽  
P. Wakonig ◽  
B. Eber ◽  
M. Mokry ◽  
...  

This case report describes a 38-year-old male who was hospitalized for further clarification of clinically mild hyperthyroidism. His increased total hormone levels, the elevated free thyroid hormones and the elevated basal TSH with blunted response to TRH strongly suggested a pituitary adenoma with inappropriate TSH incretion. Transmission computed tomography showed an intrasellar expansion, 16 mm in diameter. The neoplastic TSH production was confirmed by an elevated alpha-subunit and a raised molar alpha-sub/ATSH ratio. However, T4 distribution on prealbumin (PA, TTR), albumin (A) and thyroxine binding globulin (TBG) showed a clearly increased binding to PA (39%), indicating additional prealbumin-associated hyperthyroxinemia. The absolute values of PA, A and TBG were within the normal range. After removal of the TSH-producing adenoma, basal TSH, the free thyroid hormones and T4 binding to prealbumin returned to normal. Therefore, the prealbumin-associated hyperthyroxinemia had to be interpreted as a transitory phenomenon related to secondary hyperthyroidism (T4 shift from thyroxine binding globulin to prealbumin) rather than a genetically conditioned anomaly of protein binding.


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