Propranolol and Thyroid Hormone Metabolism

Wiersinga, W. M.

doi:10.1089/thy.1991.1.273

Cited by 51 publications

(31 citation statements)

References 47 publications

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“…Deiodinase type 1 (D1) is the principal hepatic TH deiodinating enzyme and is a major contributor to T 3 production in the rat (16). ␤-adrenergic blockers, such as propanolol, are widely used in the initial clinical management of hyperthyroid patients, in part because these drugs inhibit T 4 to T 3 conversion on the hepatic level (17). However, it is unknown if hepatic D1 activity is neurally regulated.…”

Section: Discussionmentioning

confidence: 99%

Thyroid hormone modulates glucose production via a sympathetic pathway from the hypothalamic paraventricular nucleus to the liver

Klieverik

Janssen

Riel

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

143

130

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Thyrotoxicosis increases endogenous glucose production (EGP) and induces hepatic insulin resistance. We have recently shown that these alterations can be modulated by selective hepatic sympathetic and parasympathetic denervation, pointing to neurally mediated effects of thyroid hormone on glucose metabolism. Here, we investigated the effects of central triiodothyronine (T3) administration on EGP. We used stable isotope dilution to measure EGP before and after i.c.v. bolus infusion of T3 or vehicle in euthyroid rats. To study the role of hypothalamic preautonomic neurons, bilateral T3 microdialysis in the paraventricular nucleus (PVN) was performed for 2 h. Finally, we combined T3 microdialysis in the PVN with selective hepatic sympathetic denervation to delineate the involvement of the sympathetic nervous system in the observed metabolic alterations. T3 microdialysis in the PVN increased EGP by 11 ؎ 4% (P ‫؍‬ 0.020), while EGP decreased by 5 ؎ 8% (ns) in vehicle-treated rats (T3 vs. Veh, P ‫؍‬ 0.030). Plasma glucose increased by 29 ؎ 5% (P ‫؍‬ 0.0001) after T3 microdialysis versus 8 ؎ 3% in vehicle-treated rats (T3 vs. Veh, P ‫؍‬ 0.003). Similar effects were observed after i.c.v. T3 administration. Effects of PVN T3 microdialysis were independent of plasma T3, insulin, glucagon, and corticosterone. However, selective hepatic sympathectomy completely prevented the effect of T3 microdialysis on EGP. We conclude that stimulation of T3-sensitive neurons in the PVN of euthyroid rats increases EGP via sympathetic projections to the liver, independently of circulating glucoregulatory hormones. This represents a unique central pathway for modulation of hepatic glucose metabolism by thyroid hormone.deiodinase ͉ hepatic glucose metabolism ͉ hypothalamus ͉ microdialysis ͉ sympathetic nervous system T hyroid hormones are crucial regulators of metabolism, as illustrated by the profound metabolic derangements in patients with thyrotoxicosis or hypothyroidism (1). Thyrotoxicosis is associated with an increase in endogenous glucose production (EGP), hepatic insulin resistance, and concomitant hyperglycemia (1, 2). We have recently shown that selective hepatic sympathetic denervation attenuates the hyperglycemia and increased EGP during thyrotoxicosis, while selective hepatic parasympathetic denervation aggravates hepatic insulin resistance in thyrotoxic rats. By inference, the increase in EGP during thyrotoxicosis may be mediated in part by sympathetic input to the liver, while parasympathetic hepatic input may function to restrain insulin resistance during thyrotoxicosis (3).The central nervous system is emerging as an important target for several endocrine and humoral factors in regulating metabolism. Hormones like insulin (4), estrogen (5), and corticosteroids (6) appear to use dual mechanisms to affect metabolism: that is, by direct actions in the respective target tissue and by indirect actions via the hypothalamus, in turn affecting target tissues via autonomic nervous system projections. For example, it has been convinci...

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Section: Discussionmentioning

confidence: 99%

Thyroid hormone modulates glucose production via a sympathetic pathway from the hypothalamic paraventricular nucleus to the liver

Klieverik

Janssen

Riel

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

143

130

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“…In fact, nadolol is thought to have agonistic effects at the ␤ 3 AR (29), an effect that may account for the enhanced mortality rate seen in our animals pretreated with nadolol before MDMA treatment. Because thyroid hormone is involved in MDMA-induced hyperthermia in rodents (14), we also chose to use two different nonselective ␤-blockers because of the potentially confounding hypothyroid effects of propranolol (29,30). Neither propranolol nor nadolol pretreatment altered the hyperthermic effects of MDMA.…”

Section: Discussionmentioning

confidence: 99%

Carvedilol reverses hyperthermia and attenuates rhabdomyolysis induced by 3,4-methylenedioxymethamphetamine (MDMA, Ecstasy) in an animal model*

Sprague

Moze

Caden

et al. 2005

Critical Care Medicine

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“…Other medications that may affect mood symptoms and thyroid function are beta blockers. 24 In this study, the proportion of patients receiving beta blockers was about equal in those with and without symptoms of depression; however, this proportion was significantly higher among patients without than among those with symptoms of anxiety. These data suggest that use of beta blockers had no impact on symptoms of depression and may have improved symptoms of anxiety.…”

Section: Discussionmentioning

confidence: 47%

Depression and thyroid axis function in coronary artery disease: Impact of cardiac impairment and gender

Bunevičius¹,

Varoneckas²,

Prange³

et al. 2006

Clinical Cardiology

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SummaryBackground: Increased rates of depression are reported in coronary artery disease (CAD). In heart disease, depression increases disability, reduces quality of life, and increases mortality.Hypothesis: The study was undertaken to examine the relationship between depression and thyroid axis function in patients with CAD.Methods: In all, 73 patients with CAD, consecutively admitted to a cardiac rehabilitation hospital, were assessed for depression using the Hospital Anxiety and Depression scale (HADS). Blood was drawn for assessment of thyroid axis hormones and the N-amino terminal fragment of the pro-B-type natriuretic peptide (NT-pro BNP).Results: The patients with CAD with depressive symptoms had a higher prevalence of cardiac failure (p = 0.04), higher NT-pro BNP concentrations (p = 0.02), and lower free triiodothyronine (T 3 ) concentrations (p = 0.04) than patients with CAD but without depressive symptoms. They also showed a strong trend (p = 0.058) toward a higher incidence of the low T 3 syndrome. Higher NT-pro BNP concentrations were related to lower total T 3 concentrations (r = Ϫ0.294, p = 0.011) and to higher reverse T 3 concentrations (r = 0.353, p =

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Propranolol and Thyroid Hormone Metabolism

Cited by 51 publications

References 47 publications

Thyroid hormone modulates glucose production via a sympathetic pathway from the hypothalamic paraventricular nucleus to the liver

Thyroid hormone modulates glucose production via a sympathetic pathway from the hypothalamic paraventricular nucleus to the liver

Carvedilol reverses hyperthermia and attenuates rhabdomyolysis induced by 3,4-methylenedioxymethamphetamine (MDMA, Ecstasy) in an animal model*

Depression and thyroid axis function in coronary artery disease: Impact of cardiac impairment and gender

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