Thyroid hormone-catecholamine interrelationship during cold acclimation in rats Compensatory role of catecholamine for altered thyroid states

Abstract

Effects of hyper-and hypothyroidism on catecholamine (CA) metabolism in the brain, adrenal glands, liver, and brown adipose tissue (BAT) were studied in adult rats during cold acclimation. Hypothyroidism was induced by the administration of propylthiouracil (PTU) and hyperthyroidism by the injection of thyroxine (T4). After 2 weeks of treatment, they were exposed to cold (5\s=deg\C)and sacrificed after 1 or 4 weeks. Although the body weight gain of PTU-treated rats were markedly impaired, the body temperature was maintained within normal range. They had increased cerebral dopamine, adrenal CA and BAT norepinephrine (NE) contents, enhanced cerebral tyrosine hydroxylase and adrenal dopamine \g=b\-hydroxylase (DBH) activities and elevated [3H]dihydroalprenolol (DHA) binding to liver plasma membranes (P <0.01 vs controls). T4-treated rats showed an increased brain and adrenal CA only after cold exposure. The BAT NE content, DHA binding to liver plasma membranes, and[3H]guanosine diphosphate binding to BAT mitochondria were reduced by 30 to 50% from control values after 4 weeks of cold exposure. These results indicate that during cold acclimation, 1) thyroid hormone deficiency is associated with an accelerated CA synthesis and release, which results in an enhanced BAT thermogenesis, and 2) the hyperthyroid state suppresses CA release, hepatic DHA binding, and BAT heat production. Thus, there is a close metabolic interrelationship between thyroid hormone and CA during exposure to cold. CA appears to ameliorate thyroid hormone excess or deficiency.The calorigenic action of thyroid hormone and catecholamine (CA) is well established. Both arise from the common precursor, tyrosine, and play a pivotal role in the homeotherm. Thyroid hor¬ mone controls the basal metabolic rate (BMR) by stimulating oxydative phosphorylation of the mitochondrial respiratory chain. Thyroid hor¬ mone-induced changes in BMR usually occur slowly and tend to persist. On the other hand, CA increases heat production above BMR by enhanc¬ ing lipolysis and glycolysis in response to various metabolic demands, which are rapidly switched on and off. On exposure to cold, an elevation of heat pro¬ duction is brought about by the enhanced nore¬ pinephrine (NE) secretion from the sympathetic nervous system (Hsieh et al. 1957b), which is the underlying mechanism of non-shivering thermo¬ genesis. Recently, the major site of non-shivering thermogenesis is recognized to be brown adipose tissue (BAT) (Foster & Frydman 1978). Although a line of evidence indicates that cold exposure evokes a rapid rise in plasma thyrotropin (TSH) (Knigge 1960;Itoh et al. 1966) and a stimulation of thyroid secretion, the interrelationship be¬ tween thyroid hormone and CA still remains to be elucidated. In our study, we examined effects of altered thyroid states on the CA metabolism in the central nervous system (CNS), adrenal glands, liver, and BAT during cold acclimation. We show that there is a close metabolic interrelationship between thyroid hormone and CA.

Pharmacological Activation of Thyroid Hormone Receptors Elicits a Functional Conversion of White to Brown Fat

“…In vitro , thyroid hormone, and other TR agonists including GC-1, induce thermogenic genes in brown adipocytes and are, in fact, necessary for brown adipocyte cell culture (Guerra et al 1998; Martinez de Mena et al 2010). In vivo , however, thyroid thermogenesis is generally accompanied by decreased BAT activity, indicating that the observed thermogenesis must originate from tissues other than BAT (Abelenda & Puerta 1992; Sato et al 1986). Thus, the decreased BAT activity observed with GC-1 treatment is likely not a cell autonomous effect of the compound, but is instead a result of decreased SNS innervation of BAT.…”

Myxedema madness complicating postoperative follow-up of thyroid cancer

“…The potential mechanisms of action include the interaction of thyroid hormones and neurotransmitters. It has been shown that an enhanced activity of the enzyme tyrosine hydroxylase is related to increased concentrations of dopamine (DA) in the brain of hypothyroid rats, thereby leading to the manifestation of mania due to monoamine excess (10)(11)(12). Another hypothesis is based on serotonin activity.…”

Central cooling effects in patients with hypercholesterolaemia

“…Enhanced T % outer ring deiodination in response to cold could be mediated by catecholamines. Catecholamines, which are thought to play an important role in response to cold and interact with T % during cold adaptation [35][36][37], might increase iodothyronine 5h-deiodinase activity [38]. Solter et al [33] explained that the increased serum free thyroid hormone levels imply a higher equilibrium between extracellular and intracellular FT % and FT $ as a result of prolonged intermittent cold exposure.…”