Relative roles of the thyroid hormones and noradrenaline on the thermogenic activity of brown adipose tissue in the rat

Cageao, Laura F.; Noli, M. I.; Mignone, I R; Farber, M; Ricci, C.; Hagmüller, K.; Zaninovich, Angel A.

doi:10.1677/joe.0.1450579

Cited by 9 publications

(8 citation statements)

References 16 publications

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“…Muscle and BAT mitochondria from hypothyroid rats had an 80% fall in oxygen consumption. The fall in BAT respiration resembled the effects of BAT surgical sympathectomy (6). Liver mitochondrial respiration decreased by 50% after treatment with adrenergic blockers.…”

Section: Effects Of Adrenergic-receptor Blockers In Cold-acclimated Ratsmentioning

confidence: 63%

Mitochondrial respiration in muscle and liver from cold-acclimated hypothyroid rats

Zaninovich¹,

Rebagliati²,

Raı́ces³

et al. 2003

Journal of Applied Physiology

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Zaninovich, Angel A., Iné s Rebagliati, Marcela Raíces, Conrado Ricci, and Karl Hagmü ller. Mitochondrial respiration in muscle and liver from cold-acclimated hypothyroid rats. J Appl Physiol 95: 1584-1590, 2003. First published June 27, 2003 10.1152/japplphysiol.00363.2003.-The effects of long-term cold exposure on muscle and liver mitochondrial oxygen consumption in hypothyroid and normal rats were examined. Thyroid ablation was performed after 8-wk acclimation to 4°C. Hypothyroid and normal controls remained in the cold for an additional 8 wk. At the end of 16-wk cold exposure, all hypothyroid rats were alive and normothermic and had normal body weight. At ambient temperature (24°C), thyroid ablation induced a 65% fall in muscle mitochondrial oxygen consumption, which was reversed by thyroxine but not by norepinephrine administration. After cold acclimation was reached, suppression of thyroid function reduced muscle mitochondrial respiration by 30%, but the hypothyroid values remained about threefold higher than those in hypothyroid muscle in the warm. Blockade of ␤-and ␣1-adrenergic receptors in both hypothyroid and normal rats produced hypothermia in vivo and a fall in muscle, liver, and brown adipose tissue mitochondria respiration in vitro. In normal rats, cold acclimation enhanced muscle respiration by 35%, in liver 18%, and in brown adipose tissue 450% over values in the warm. The results demonstrate that thyroid hormones, in the presence of norepinephrine, are major determinants of thermogenic activity in muscle and liver of cold-acclimated rats. After thyroid ablation, cold-induced nonshivering thermogenesis replaced 3,5,3Ј-triiodothyronine-induced thermogenesis, and normal body temperature was maintained. cold acclimation; oxygen consumption; norepinephrine; adrenergic-receptor blockers ENDOTHERMIC ANIMALS LIVING in a cold environment maintain normothermia and energy balance through an activation of mechanisms that increase heat production and heat conservation. Heat production is commonly classified as either obligatory or adaptive (for reviews, see Refs. 15,23,29,38). The obligatory thermogenesis results from the widespread metabolic activity in many tissues and serves to maintain normal body temperature, which in homeotherms is usually higher than ambient temperature. The thyroid hormones stimulate obligatory thermogenesis by a number of mechanisms that are still incompletely understood (8,32,38). The additional heat needed to preserve body temperature in a cold environment is obtained through adaptive or facultative thermogenesis, a process regulated by the hypothalamus through the sympathetic nervous system. Brown adipose tissue (BAT) is the main site for adaptive thermogenesis primarily because of the mitochondrial uncoupling protein-1 (UCP-1), which uncouples electron transport from the phosphorylation of ADP and appears to be the only protein able to respond to thermal challenge (31, 30).UCP-1 expression is stimulated by norepinephrine (NE) but requires the presence of thyroid hormones (3, 4,...

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Section: Effects Of Adrenergic-receptor Blockers In Cold-acclimated Ratsmentioning

confidence: 63%

Mitochondrial respiration in muscle and liver from cold-acclimated hypothyroid rats

Zaninovich¹,

Rebagliati²,

Raı́ces³

et al. 2003

Journal of Applied Physiology

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“…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: 95%

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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“…Groups of normal rats were subjected to excision of the 5 sympathetic nerves supplying each BAT lobe, as described in an earlier report (11). The respective control rats were subjected to sham operations.…”

Section: Experiments 1: Effects Of Cold Exposure and Sx On Bat Npymentioning

confidence: 99%

NEUROPEPTIDE Y SUPPRESSED THE T₃-INDUCED RISE IN BROWN FAT MITOCHONDRIAL RESPIRATION IN HYPOTHYROID RATS

et al. 2001

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It has been postulated that a cold-induced decrease in hypothalamic neuropeptide Y (NPY) might disinhibit the sympathetic outflow that activates brown adipose tissue (BAT) thermogenesis. The present work has assessed the interscapular BAT NPY and norepinephrine (NE) concentrations 7 days after surgical excision of the sympathetic nerves (Sx) of each BAT lobe in rats exposed to 4 degrees C or 24 degrees C during 24 h. In addition, the effects of NPY treatment on BAT oxygen (O2) consumption in normal and T3-treated hypothyroid rats was determined. Sprague-Dawley rats weighing 220-240 g were used. BAT was removed and homogenized in 0.1 M HCl. BAT NPY content at 24 degrees C was 109 +/- 19 pg/mg protein. Sx decreased this value significantly (P < 0.001) and cold increased it by two-fold (P < 0.001). Neither cold nor Sx altered hypothalamic NPY. BAT O2 consumption was depressed by NPY treatment (P < 0.001) and increased by NE (P < 0.001). In euthyroid Sx rats, NPY decreased O2 consumption (P < 0.001). NPY failed to alter O2 consumption in hypothyroid rats and sharply decreased it in T3-treated rats. The results show that NPY blocked the effects of T3 on BAT O2 consumption, and that cold-induced activation of the thermogenic process did not produce measurable changes in hypothalamic NPY.

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Relative roles of the thyroid hormones and noradrenaline on the thermogenic activity of brown adipose tissue in the rat

Cited by 9 publications

References 16 publications

Mitochondrial respiration in muscle and liver from cold-acclimated hypothyroid rats

Mitochondrial respiration in muscle and liver from cold-acclimated hypothyroid rats

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

NEUROPEPTIDE Y SUPPRESSED THE T₃-INDUCED RISE IN BROWN FAT MITOCHONDRIAL RESPIRATION IN HYPOTHYROID RATS

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Relative roles of the thyroid hormones and noradrenaline on the thermogenic activity of brown adipose tissue in the rat

Cited by 9 publications

References 16 publications

Mitochondrial respiration in muscle and liver from cold-acclimated hypothyroid rats

Mitochondrial respiration in muscle and liver from cold-acclimated hypothyroid rats

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

NEUROPEPTIDE Y SUPPRESSED THE T3-INDUCED RISE IN BROWN FAT MITOCHONDRIAL RESPIRATION IN HYPOTHYROID RATS

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NEUROPEPTIDE Y SUPPRESSED THE T₃-INDUCED RISE IN BROWN FAT MITOCHONDRIAL RESPIRATION IN HYPOTHYROID RATS