Effects of hypothyroidism and hyperthyroidism on GDP binding to brown-adipocyte mitochondria from rats

Woodward, Jonathan; Saggerson, E D

doi:10.1042/bj2630341

Cited by 7 publications

(3 citation statements)

References 37 publications

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“…One of the early reports by Silva et al demonstrated that both cold exposure and sympathetic activation could induce hyperactivation of type II iodothyronine 5'-deiodinase (17). Furthermore, a positive effect of TH on GDP binding, uncoupling protein-1 expression, and cAMPinducible type II deiodinase has been reported (18,19). Thus until now, little is known about the effects of TH in human BAT, considering the significant differences in adipose tissues between rodents and humans.…”

Section: Discussionmentioning

confidence: 99%

Activation of brown adipose tissue in hypothyroidism

et al. 2015

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Section: Discussionmentioning

confidence: 99%

Activation of brown adipose tissue in hypothyroidism

et al. 2015

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“…In itself, this hyperpyrexia, as all hyperpyrexias (see sect. VE2), should lead to some recruitment and activation of brown adipose tissue; brown fat-derived heat would be optional for the process, and several (although not all, see below) reports do indicate recruitment of brown adipose tissue in hyperthyroidism (49,364,690,778,871).…”

Section: Thyroid Thermogenesismentioning

confidence: 99%

Brown Adipose Tissue: Function and Physiological Significance

Cannon

Nedergaard

2004

Physiological Reviews

5,545

126

5,981

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The function of brown adipose tissue is to transfer energy from food into heat; physiologically, both the heat produced and the resulting decrease in metabolic efficiency can be of significance. Both the acute activity of the tissue, i.e., the heat production, and the recruitment process in the tissue (that results in a higher thermogenic capacity) are under the control of norepinephrine released from sympathetic nerves. In thermoregulatory thermogenesis, brown adipose tissue is essential for classical nonshivering thermogenesis (this phenomenon does not exist in the absence of functional brown adipose tissue), as well as for the cold acclimation-recruited norepinephrine-induced thermogenesis. Heat production from brown adipose tissue is activated whenever the organism is in need of extra heat, e.g., postnatally, during entry into a febrile state, and during arousal from hibernation, and the rate of thermogenesis is centrally controlled via a pathway initiated in the hypothalamus. Feeding as such also results in activation of brown adipose tissue; a series of diets, apparently all characterized by being low in protein, result in a leptin-dependent recruitment of the tissue; this metaboloregulatory thermogenesis is also under hypothalamic control. When the tissue is active, high amounts of lipids and glucose are combusted in the tissue. The development of brown adipose tissue with its characteristic protein, uncoupling protein-1 (UCP1), was probably determinative for the evolutionary success of mammals, as its thermogenesis enhances neonatal survival and allows for active life even in cold surroundings.

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“…Given that response elements for thyroid hormone receptors have been identified in the UCP1 gene promoter (Silva & Rabelo 1997), it is not surprising that alterations in BAT nuclear thyroid receptor occupancy levels produce substantial changes in UCP1 concentration. Thus, hyperthyroidism produced by T 3 treatment significantly increased UCP1 mRNA levels (Masaki et al 1997), UCP1 content (Branco et al 1999), and guanosine 5 -diphosphate (GDP) binding to brown-adipocyte mitochondria (Woodward & Saggerson 1989). On the other hand, the effects of T 4 on BAT UCP1 levels are still controversial.…”

Section: Introductionmentioning

confidence: 97%

Thyroxine and tri-iodothyronine differently affect uncoupling protein-1 content and antioxidant enzyme activities in rat interscapular brown adipose tissue

Petrovič

Cvijic̀²,

Davidović³

2003

Journal of Endocrinology

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The activity of the antioxidant enzymes copper-zinc superoxide dismutase (CuZnSOD), manganese superoxide dismutase (MnSOD) and catalase (CAT), as well as mitochondrial glycerol-3-phosphate dehydrogenase (mGPDH) activity, uncoupling protein-1 (UCP1) content, catecholamine degrading enzyme monoamine oxidase (MAO) activity and malonyl dialdehyde (MDA) concentration were studied in rat interscapular brown adipose tissue (IBAT). Rats were treated with either thyroxine (T 4 ) or tri-iodothyronine (T 3 ) for five days and then exposed to cold (4 C, 24 h) or housed at room temperature (22 C). Under basal conditions, T 3 treatment significantly increased UCP1 content and MnSOD activity whereas CuZnSOD, CAT and MAO activities were significantly decreased. Thyroxine treatment significantly decreased IBAT CAT activity while MDA levels markedly increased. Cold exposure induced a significant augmentation of UCP1 content and MnSOD and mGPDH activities only in animals that were rendered hyperthyroid by T 4 treatment. In T 3 -treated animals acutely exposed to cold stress, MDA concentration, an indicator of lipid peroxidation, was significantly higher compared with that of T 3 -treated animals housed at room temperature. However, in T 4 -treated animals, MDA concentrations were markedly lower. These results show that T 4 and T 3 differently affect IBAT parameters studied not only under basal but also under cold-stimulated conditions.

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Effects of hypothyroidism and hyperthyroidism on GDP binding to brown-adipocyte mitochondria from rats

Cited by 7 publications

References 37 publications

Activation of brown adipose tissue in hypothyroidism

Activation of brown adipose tissue in hypothyroidism

Brown Adipose Tissue: Function and Physiological Significance

Thyroxine and tri-iodothyronine differently affect uncoupling protein-1 content and antioxidant enzyme activities in rat interscapular brown adipose tissue

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