Effects of thyroid hormones on mitochondrial oxygen consumption in brown adipose tissue and heart from cold-exposed hypothyroid rats

Lf, Cageao; Mignone, I R; Ricci, C.; Brignone, C.C. De; Brignone, J.A.; Zaninovich, Angel A.

doi:10.1530/acta.0.1270072

Cited by 11 publications

(9 citation statements)

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“…In fact, Table 1 shows that the ␣-GPD activity in the BAT of hypothyroid rats was Ͼ230 times higher than that in liver, which accounts for the enhanced substrate oxidations in BAT mitochondria. In a previous study (6), BAT ␣-GPD activity was 15-fold that in heart, and it was not affected by changes in temperature or thyroid hormones.…”

Section: Changes In ␣-Gpd Activitymentioning

confidence: 55%

“…This degree of receptor occupancy could not be reached in cold-exposed, T 3 -treated hypothyroid rats even after the administration of Ͼ15 times the physiological T 3 replacement and extremely hyperthyroid levels of serum T 3 (3). This phenomenon explains the development of hypothermia during cold exposure of hypothyroid rats treated with physiological amounts of T 3 (6,7). The foregoing data are consistent with the fact that thyroid hormone production in hypothyroid rats was nil or sufficiently low that it resulted in a deep hypothyroid state.…”

Section: Discussionmentioning

confidence: 96%

See 1 more Smart Citation

Brown fat thermogenesis in cold-acclimated rats is not abolished by the suppression of thyroid function

Zaninovich¹,

Raı́ces

Rebagliati³

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

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-The effects of long-term cold exposure on brown adipose tissue (BAT) thermogenesis in hypothyroid rats have been examined. Thyroid ablation was performed in normal rats after 2 mo of exposure to 4°C, when BAT hypertrophy and thermogenic activity were maximal. After ablation, hypothyroid and normal controls remained in the cold for 2 additional months. At the end of the 4-mo cold exposure, all untreated hypothyroid rats were alive, had normal body temperature, and had gained an average 12.8% more weight than normal controls. Long-term cold exposure of hypothyroid rats markedly increased BAT weight, mitochondrial proteins, uncoupling protein (UCP)-1, mRNA for UCP-1, and oxygen consumption to levels similar to those seen in cold-exposed normal rats. The results indicate that thyroid hormones are required for increased thermogenic capacity to occur as an adaptation to long-term cold exposure. However, cold adaptation can be maintained in the absence of thyroid hormone. cold acclimation; uncoupling protein-1; hypothyroidism; oxygen consumption; norepinephrine THE IMPORTANCE OF THE BROWN ADIPOSE TISSUE (BAT) thermogenic response to acute cold stress has been widely recognized (for reviews see Refs. 21,22,30). Numerous complex phenomena take place in BAT after exposure to low temperatures, leading to the synthesis of mitochondrial proteins involved in heat production. A critical role in this process is the synthesis of uncoupling protein-1 (UCP-1), strongly promoted by norepinephrine (NE) through a synergism between ␣-and ␤-adrenergic receptors (24,32,40). The presence of the thyroid hormones is essential to initiate BAT heat production, because triiodothyronine (T 3 ) potentiates the action of NE on UCP-1 gene transcription (2-4, 37). This explains the development of hypothermia in hypothyroid rats soon after exposure to low temperatures, an effect corrected by the administration of thyroid hormones but not by the administration of NE (39).Thyroid hormones are active regulators of basal metabolic rate (BMR) and energy expenditure by a number of mechanisms (9,12,38,39). However, earlier studies had suggested that the thyroid hormone may not be necessary for a sustained normothermia after acclimation to cold has been achieved (for review see Ref. 13). Thus Hsieh and Carlson (25) observed a high metabolic rate and normal life survival in hypothyroid rats adapted to cold before thyroidectomy. Despite numerous studies, the influence of thyroid function on the maintenance of normothermia in rodents exposed to prolonged low temperature is not clearly understood.The purpose of the present study was to assess the role of the thyroid hormones in BAT thermogenesis during long-term cold exposure. After a period of time in the cold, rats were made hypothyroid. Hypothyroid and normal controls were then maintained for an additional period of time in the cold, and thereafter BAT was studied. Accordingly, hypothyroidism was induced after BAT hypertrophy and thermogenic activity were maximally activated. In contrast, room temperaturea...

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Section: Changes In ␣-Gpd Activitymentioning

confidence: 55%

Section: Discussionmentioning

confidence: 96%

Brown fat thermogenesis in cold-acclimated rats is not abolished by the suppression of thyroid function

Zaninovich¹,

Raı́ces

Rebagliati³

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

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“…Conversely, other factors, exhibiting different serum concentrations in functional and experimental hyperthyroidism, should be involved in mitochondrial proliferation associated to cold exposure. Unlike cold exposure, T 3 administration strongly decreases serum levels of T 4 , (Venditti et al, 2006a), which has been reported to have intrinsic biological activity in the cold (Cageao et al, 1992). Plasma levels of catecholamines, which are not modified in altered thyroid states (Stoffer et al, 1973), remarkably increase during cold exposure (Storm et al, 1981).…”

Section: Introductionmentioning

confidence: 98%

Involvement of PGC-1, NRF-1, and NRF-2 in metabolic response by rat liver to hormonal and environmental signals

Venditti

Bari

Stefano

et al. 2009

Molecular and Cellular Endocrinology

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.Page 1 AbstractWe studied liver oxidative capacity and O 2 consumption in hypothyroid rats treated for 10 days with T 4 , or T 3 , or treated for 10 days with T 3 and exposed to cold for the last two days. The metabolic response of homogenates and mitochondria indicated that all treatments increased the synthesis of respiratory chain components, whereas only the cold induced mitochondrial proliferation. Determination of mRNA and protein expression of transcription factor activators, such as NRF-1 and NRF-2, and coactivators, such as PGC-1, showed that mRNA levels, except PGC-1 ones, were not related to aerobic capacities. Conversely, a strong correlation was found was between cytochrome oxidase activity and PGC-1 or NRF-2 protein levels.Such a correlation was not found for NRF-1. Our results strongly support the view that in rat liver PGC-1 and NRFs are responsible for the iodothyronine-induced increases in respiratory chain components, whereas their role in cold-induced mitochondrial proliferation needs to be further on clarified.

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“…However, only data concerning changes in glutathione peroxidase activity and mitochondrial protein content favour the idea that dissimilarities in effects of cold exposure and T 3 treatment could depend on differences in serum levels of T 4 . the cold (Cageao et al, 1992). Thus, it is possible that T 4 contributes to some changes underlying tissue thermogenesis and oxidative stress associated with cold exposure.…”

Section: Introductionmentioning

confidence: 99%

Differential effects of experimental and cold-induced hyperthyroidism on factors inducing rat liver oxidative damage

Venditti¹,

Pamplona

Ayala

et al. 2006

Journal of Experimental Biology

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SUMMARY Thyroid hormone-induced increase in metabolic rates is often associated with increased oxidative stress. The aim of the present study was to investigate the contribution of iodothyronines to liver oxidative stress in the functional hyperthyroidism elicited by cold, using as models cold-exposed and 3,5,3′-triiodothyronine (T3)- or thyroxine(T4)-treated rats. The hyperthyroid state was always associated with increases in both oxidative capacity and oxidative damage of the tissue. The most extensive damage to lipids and proteins was found in T3-treated and cold-exposed rats, respectively. Increase in oxygen reactive species released by mitochondria and microsomes was found to contribute to tissue oxidative damage, whereas the determination of single antioxidants did not provide information about the possible contribution of a reduced effectiveness of the antioxidant defence system. Indeed, liver oxidative damage in hyperthyroid rats was scarcely related to levels of the liposoluble antioxidants and activities of antioxidant enzymes. Conversely,other biochemical changes, such as the degree of fatty acid unsaturation and hemoprotein content, appeared to predispose hepatic tissue to oxidative damage associated with oxidative challenge elicited by hyperthyroid state. As a whole, our results confirm the idea that T3 plays a key role in metabolic changes and oxidative damage found in cold liver. However,only data concerning changes in glutathione peroxidase activity and mitochondrial protein content favour the idea that dissimilarities in effects of cold exposure and T3 treatment could depend on differences in serum levels of T4.

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Effects of thyroid hormones on mitochondrial oxygen consumption in brown adipose tissue and heart from cold-exposed hypothyroid rats

Cited by 11 publications

References 0 publications

Brown fat thermogenesis in cold-acclimated rats is not abolished by the suppression of thyroid function

Brown fat thermogenesis in cold-acclimated rats is not abolished by the suppression of thyroid function

Involvement of PGC-1, NRF-1, and NRF-2 in metabolic response by rat liver to hormonal and environmental signals

Differential effects of experimental and cold-induced hyperthyroidism on factors inducing rat liver oxidative damage

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