Reduction of thyroid hormones triggers down-regulation of hepatic CYP2B through nuclear receptors CAR and TR in a rat model of acute stroke

Bing, Yuntao; Zhu, Siying; Jiang, Kun; Dong, Guicheng; Li, Jie; Yang, Zhongxue; Yang, Jing; Yue, Jiang

doi:10.1016/j.bcp.2013.12.011

Cited by 14 publications

(10 citation statements)

References 38 publications

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“…Beyond this, studies elucidated that CAR is also linked to hepatic lipid and glucose metabolism (Wada et al 2009;Xiao et al 2013). In vitro data from the hepatic Huh7 cell line and cryopreserved small hepatocytes have shown that TH may regulate the expression of specific CAR target genes possibly by binding of the activated TH receptor to the PBREM region (Ooe et al 2009, Bing et al 2014. In addition, it was shown that CAR itself can regulate the TH responsive gene Thrsp through binding to TRE sequences of the promoter region (Breuker et al 2010).…”

Section: -T 2 Alters Murine Genesmentioning

confidence: 99%

3,5-T2 alters murine genes relevant for xenobiotic, steroid, and thyroid hormone metabolism

Lietzow

Golchert

Homuth

et al. 2016

Journal of Molecular Endocrinology

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The endogenous thyroid hormone (TH) metabolite 3,5-diiodo-l-thyronine (3,5-T 2 ) acts as a metabolically active substance affecting whole-body energy metabolism and hepatic lipid handling in a desirable manner. Considering possible adverse effects regarding thyromimetic action of 3,5-T 2 treatment in rodents, the current literature remains largely controversial. To obtain further insights into molecular mechanisms and to identify novel target genes of 3,5-T 2 in liver, we performed a microarray-based liver tissue transcriptome analysis of male lean and diet-induced obese euthyroid mice treated for 4 weeks with a dose of 2.5 µg/g bw 3,5-T 2 . Our results revealed that 3,5-T 2 modulates the expression of genes encoding Phase I and Phase II enzymes as well as Phase III transporters, which play central roles in metabolism and detoxification of xenobiotics. Additionally, 3,5-T 2 changes the expression of TH responsive genes, suggesting a thyromimetic action of 3,5-T 2 in mouse liver. Interestingly, 3,5-T 2 in obese but not in lean mice influences the expression of genes relevant for cholesterol and steroid biosynthesis, suggesting a novel role of 3,5-T 2 in steroid metabolism of obese mice. We concluded that treatment with 3,5-T 2 in lean and diet-induced obese male mice alters the expression of genes encoding hepatic xenobiotic-metabolizing enzymes that play a substantial role in catabolism and inactivation of xenobiotics and TH and are also involved in hepatic steroid and lipid metabolism. The administration of this high dose of 3,5-T 2 might exert adverse hepatic effects. Accordingly, the conceivable use of 3,5-T 2 as pharmacological hypolipidemic agent should be considered with caution.3,5-T 2 alters murine genes relevant for xenobiotic, steroid, and thyroid hormone metabolism

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Section: -T 2 Alters Murine Genesmentioning

confidence: 99%

3,5-T2 alters murine genes relevant for xenobiotic, steroid, and thyroid hormone metabolism

Lietzow

Golchert

Homuth

et al. 2016

Journal of Molecular Endocrinology

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“…[ 24 ] Furthermore, low fT3 levels may induce the down-regulation of hepatic CYP2B1 in stroke model, which mediates metabolism of exogenous and endogenous substances. [ 25 ] All of these can affect recovery of neurological function after stroke.…”

Section: Discussionmentioning

confidence: 99%

Low free triiodothyronine levels predict symptomatic intracranial hemorrhage and worse short-term outcome of thrombolysis in patients with acute ischemia stroke

2017

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The aim of the study was to determine whether thyroid hormones level on admission in patients with ischemic stroke, treated with intravenous recombinant tissue type plasminogen activator (rtPA), was associated with symptomatic intracranial hemorrhage (sICH) and worse outcomes at 3 months.Patients with acute ischemic stroke (AIS) receiving intravenous rtPA thrombolytic treatment on our stroke unit between January 2015 and June 2016 were included in this study. Serum-free triiodothyronine (fT3), free thyroxine (fT4), total triiodothyronine (tT3), total thyroxine (tT4), and thyroid-stimulating hormone (TSH) were detected on admission. The endpoints were sICH, and poor functional outcomes at 3 and 6 months.In all, 159 patients (106 males; mean age 65.36 ± 10.02 years) were included. FT3 was independently associated with sICH (odds ratio [OR] 0.204, 95% confidence interval [CI] 0.065–0.642) and poor outcomes at 3 months (OR 0.396, 95% CI 0.180–1.764). The cut-off values of fT3 for sICH was 3.54 pg/mL (sensitivity 83%; specificity 83%; area under the curve 0.88). FT3 values ≤3.54 pg/mL increased risk for sICH by 3.16-fold (95% CI 0.75–1.0) compared with fT3 values >3.54 pg/mL.Low fT3 levels at admission were independently associated with sICH and worse outcomes at 3 months in AIS patients receiving rtPA thrombolytic therapy.

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“…Thyroid hormone levels in patients with ischemic stroke are reduced [ 64 ] and associated with a poorer functional prognosis to some extent [ 65 ]. Whether IPostC can increase the thyroxin levels and accelerate the clearance of Glu in CNS resulting in neuroprotection is worth further study.…”

Section: Ischemic Postconditioning May Enable the Interaction Betwmentioning

confidence: 99%

Cerebral Ischemic Postconditioning Plays a Neuroprotective Role through Regulation of Central and Peripheral Glutamate

You

Feng

Xin

et al. 2018

BioMed Research International

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Following cerebral ischemia/reperfusion (I/R) injury, a series of pathophysiological processes are stimulated in both the central nervous system (CNS) and the periphery, including, but not limited to, the peripheral immune and endocrine systems and underregulation of the neuroendocrine-immune network. Glutamate (Glu) is an important excitatory neurotransmitter in the CNS; its excitotoxicity following cerebral ischemia has been a focus of study for several decades. In addition, as a novel immunoregulator, Glu also regulates immune activity in both the CNS and periphery and may connect the CNS and periphery through regulation of the neuroendocrine-immune network. Ischemic postconditioning (IPostC) is powerful and activates various endogenous neuroprotective mechanisms following cerebral I/R, but only a few studies have focused on the mechanisms associated with Glu to date. Given that Glu plays an important and complex pathophysiological role, the understanding of Glu-related mechanisms of IPostC is an interesting area of research, which we review here.

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Reduction of thyroid hormones triggers down-regulation of hepatic CYP2B through nuclear receptors CAR and TR in a rat model of acute stroke

Cited by 14 publications

References 38 publications

3,5-T2 alters murine genes relevant for xenobiotic, steroid, and thyroid hormone metabolism

3,5-T2 alters murine genes relevant for xenobiotic, steroid, and thyroid hormone metabolism

Low free triiodothyronine levels predict symptomatic intracranial hemorrhage and worse short-term outcome of thrombolysis in patients with acute ischemia stroke

Cerebral Ischemic Postconditioning Plays a Neuroprotective Role through Regulation of Central and Peripheral Glutamate

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