Selenium and iodine deficiencies: effects on brain and brown adipose tissue selenoenzyme activity and expression

1997 ◽  
Vol 155 (2) ◽  
pp. 255-263 ◽  
Author(s):  
JH Mitchell ◽  
F Nicol ◽  
GJ Beckett ◽  
Keyword(s):  
Adipose Tissue ◽  
Thyroid Hormone ◽  
Glutathione Peroxidase ◽  
Brown Adipose Tissue ◽  
Iodine Deficiency ◽  
Uncoupling Protein ◽  
Compensatory Mechanisms ◽  
Iodothyronine Deiodinase ◽  
Brown Adipose ◽  
The Brain

Adequate dietary iodine supplies and thyroid hormones are needed for the development of the central nervous system (CNS) and brown adipose tissue (BAT) function. Decreases in plasma thyroxine (T4) concentrations may increase the requirement for the selenoenzymes types I and II iodothyronine deiodinase (ID-I and ID-II) in the brain and ID-II in BAT to protect against any fall in intracellular 3,3',5 tri-iodothyronine (T3) concentrations in these organs. We have therefore investigated selenoenzyme activity and expression and some developmental markers in brain and BAT of second generation selenium- and iodine-deficient rats. Despite substantial alterations in plasma thyroid hormone concentrations and thyroidal and hepatic selenoprotein expression in selenium and iodine deficiencies, ID-I, cytosolic glutathione peroxidase (cGSHPx) and phospholipid hydroperoxide glutathione peroxidase (phGSHPx) activities and expression remained relatively constant in most brain regions studied. Additionally, brain and pituitary ID-II activities were increased in iodine deficiency regardless of selenium status. This can help maintain tissue T3 concentrations in hypothyroidism. Consistent with this, no significant effects of iodine or selenium deficiency on the development of the brain were observed, as assessed by the activities of marker enzymes. In contrast, BAT from selenium- and iodine deficient rats had impaired thyroid hormone metabolism and less uncoupling protein than in tissue from selenium- and iodine-supplemented animals. Thus, the effects of selenium and iodine deficiency on the brain are limited due to the activation of the compensatory mechanisms but these mechanisms are less effective in BAT.

Effect of selenium and iodine deficiency on the level of uncoupling protein in brown adipose tissue of rats

1990 ◽  
Vol 18 (6) ◽  
pp. 1269-1270 ◽  
Author(s):  
ALAIN GÉLOËN ◽  
JOHN R. ARTHUR ◽  
GEOFFREY J. BECKETT ◽  
PAUL TRAYHURN
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Iodine Deficiency ◽  
Uncoupling Protein ◽  
Brown Adipose

scholarly journals Postnatal overnutrition programs the thyroid hormone metabolism and function in adulthood

2015 ◽  
Vol 226 (3) ◽  
pp. 219-226 ◽  
Author(s):  
Patricia C Lisboa ◽  
Ellen P S Conceição ◽  
Elaine de Oliveira ◽  
Egberto G Moura
Keyword(s):  
Adipose Tissue ◽  
Thyroid Hormone ◽  
Litter Size ◽  
Uncoupling Protein ◽  
Biological Significance ◽  
Adult Life ◽  
Leptin Resistance ◽  
Long Term Effects ◽  
Iodothyronine Deiodinase ◽  
Brown Adipose

Early overnutrition (EO) during lactation leads to obesity, leptin resistance and lower thyroid hormone (TH) levels during adulthood. To better understand the biological significance of this thyroid hypofunction, we studied the long-term effects of postnatal EO on both the function of hypothalamic–pituitary–thyroid (HPT) axis and the metabolism and action of TH. To induce EO, the litter size was reduced to three pups per litter (small litter (SL) group) on the third day of lactation. In the controls (normal litter group), litter size was adjusted to 10 pups per litter. Rats were killed at PN180. TRH content andin vitroTSH were evaluated. Iodothyronine deiodinase (D1 and D2) activities were measured in different tissues. Mitochondrial α-glycerol-3-phosphate dehydrogenase (mGPD), uncoupling protein 1 (UCP1) and TH receptor (TRβ1) were evaluated to assess TH action. The SL group presented lower TRH, intra-pituitary and released TSH levels, despite unchanged plasma TSH. They presented lower D1 activity in thyroid, muscle and white adipose tissue (WAT) and higher D2 activity in the hypothalamus, pituitary, brown adipose tissue (BAT) and WAT, which confirmed the hypothyroidism. UCP1 in BAT and TRβ1 in WAT were decreased, which can contribute to a lower catabolic status. Despite the lower TH, the D2 activity in the thyroid, heart and testes was unchanged. Hepatic D1, mGPD and TRβ1 were also unchanged in SL rats, suggesting that the TH conversion and action were preserved in the liver, even with lower TH. Thus, this model indicates that postnatal EO changes thyroid function in adult life in a tissue-specific way, which can help in the understanding of obesogenesis.

Thyroid-stimulating hormone receptor in brown adipose tissue is involved in the regulation of thermogenesis

2008 ◽  
Vol 295 (2) ◽  
pp. E514-E518 ◽  
Author(s):  
Toyoshi Endo ◽  
Tetsuro Kobayashi
Keyword(s):  
Adipose Tissue ◽  
Thyroid Hormone ◽  
Brown Adipose Tissue ◽  
Rectal Temperature ◽  
Hormone Receptor ◽  
Uncoupling Protein ◽  
Thyroid Stimulating Hormone ◽  
Adipose Tissues ◽  
Brown Adipose ◽  
Stimulating Hormone

C.RF- Tshrhyt/hyt mice have a mutated thyroid-stimulating hormone receptor (TSHR), and, without thyroid hormone supplementation, these mice develop severe hypothyroidism. When hypothyroid Tshrhyt/hyt mice were exposed to cold (4°C), rectal temperature rapidly dropped to 23.9 ± 0.40°C at 90 min, whereas the wild-type mice temperatures were 37.0 ± 0.15°C. When we carried out functional rat TSHR gene transfer in the brown adipose tissues by plasmid injection combined with electroporation, there was no effect on the serum levels of thyroxine, although rectal temperature of the mice transfected with pcDNA3.1/Zeo-rat TSHR 90 min after cold exposure remained at 34.6 ± 0.34°C, which was significantly higher than that of Tshrhyt/hyt mice. Transfection of TSHR cDNA increased mRNA and protein levels of uncoupling protein-1 (UCP-1) in brown adipose tissues, and the weight ratio of brown adipose tissue to overall body weight also increased. Exogenous thyroid hormone supplementation to Tshrhyt/hyt mice restored rectal temperature 90 min after exposure to cold (36.8 ± 0.10°C). These results indicate that not only thyroid hormone but also thyroid-stimulating hormone (TSH)/TSHR are involved in the expression mechanism of UCP-1 in mouse brown adipose tissue. TSH stimulates thermogenesis and functions to protect a further decrease in body temperature in the hypothyroid state.

scholarly journals Thyrotropin Receptors in Brown Adipose Tissue: Thyrotropin Stimulates Type II Iodothyronine Deiodinase and Uncoupling Protein-1 in Brown Adipocytes*

Endocrinology ◽  
2001 ◽  
Vol 142 (3) ◽  
pp. 1195-1201 ◽  
Author(s):  
Masami Murakami ◽  
Yuji Kamiya ◽  
Tadashi Morimura ◽  
Osamu Araki ◽  
Makoto Imamura ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Uncoupling Protein ◽  
Type Ii ◽  
Uncoupling Protein 1 ◽  
Iodothyronine Deiodinase ◽  
Brown Adipocytes ◽  
Brown Adipose

scholarly journals Thyroid hormones in the regulation of brown adipose tissue thermogenesis

2021 ◽  
Author(s):  
Sarah Christine Sentis ◽  
Rebecca Oelkrug ◽  
Jens Mittag
Keyword(s):  
Adipose Tissue ◽  
Thyroid Hormone ◽  
Brown Adipose Tissue ◽  
Heat Loss ◽  
Current Knowledge ◽  
Uncoupling Protein ◽  
Sympathetic Stimulation ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis ◽  
Key Aspects

A normal thyroid status is crucial for body temperature homeostasis, as thyroid hormone regulates both heat loss and conservation as well as heat production in thermogenic tissues. Brown adipose tissue (BAT) is the major site of non-shivering thermogenesis and an important target of thyroid hormone action. Thyroid hormone not only regulates the tissue’s sensitivity to sympathetic stimulation by norepinephrine, but also the expression of uncoupling protein 1, the key driver of BAT thermogenesis. Vice versa, sympathetic stimulation of BAT triggers the expression of deiodinase type II, an enzyme that enhances local thyroid hormone availability and signaling. This review summarizes the current knowledge on how thyroid hormone controls BAT thermogenesis, aiming to dissect the direct actions of the hormone in BAT and its indirect actions via the central nervous system, browning of white adipose tissue or heat loss over body surfaces. Of particular relevance is the apparent dose dependency of the observed effects, as we find that minor or moderate changes in thyroid hormone levels often have different effects as compared to high pharmacological doses. Moreover, we conclude that the more recent findings require a reevaluation of older studies, as key aspects such as heat loss or central BAT activation may not have received the necessary attention during the interpretation of these early findings. Finally, we provide a list of what we believe are the most relevant questions in the field that to date are still enigmatic and require further studies.

scholarly journals A single mutation in uncoupling protein of rat brown adipose tissue mitochondria abolishes GDP sensitivity of H+ transport.

1994 ◽  
Vol 269 (10) ◽  
pp. 7435-7438
Author(s):  
D.L. Murdza-Inglis ◽  
M. Modriansky ◽  
H.V. Patel ◽  
G. Woldegiorgis ◽  
K.B. Freeman ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Uncoupling Protein ◽  
Single Mutation ◽  
Brown Adipose

scholarly journals TAF7L modulates brown adipose tissue formation

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Haiying Zhou ◽  
Bo Wan ◽  
Ivan Grubisic ◽  
Tommy Kaplan ◽  
Robert Tjian
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Core Promoter ◽  
Uncoupling Protein ◽  
Dna Looping ◽  
Chromatin Interactions ◽  
Brown Adipose ◽  
Important Regulator

Brown adipose tissue (BAT) plays an essential role in metabolic homeostasis by dissipating energy via thermogenesis through uncoupling protein 1 (UCP1). Previously, we reported that the TATA-binding protein associated factor 7L (TAF7L) is an important regulator of white adipose tissue (WAT) differentiation. In this study, we show that TAF7L also serves as a molecular switch between brown fat and muscle lineages in vivo and in vitro. In adipose tissue, TAF7L-containing TFIID complexes associate with PPARγ to mediate DNA looping between distal enhancers and core promoter elements. Our findings suggest that the presence of the tissue-specific TAF7L subunit in TFIID functions to promote long-range chromatin interactions during BAT lineage specification.

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