Academic literature on the topic 'T1AM'

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Journal articles on the topic "T1AM"

1

Rogowski, Michael, Lorenza Bellusci, Martina Sabatini, et al. "Lipolytic Effects of 3-Iodothyronamine (T1AM) and a Novel Thyronamine-Like Analog SG-2 through the AMPK Pathway." International Journal of Molecular Sciences 20, no. 16 (2019): 4054. http://dx.doi.org/10.3390/ijms20164054.

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3-Iodothyronamine (T1AM) and its synthetic analog SG-2 are rapidly emerging as promising drivers of cellular metabolic reprogramming. Our recent research indicates that in obese mice a sub-chronic low dose T1AM treatment increased lipolysis, associated with significant weight loss independent of food consumption. The specific cellular mechanism of T1AM’s lipolytic effect and its site of action remains unknown. First, to study the mechanism used by T1AM to gain entry into cells, we synthesized a fluoro-labeled version of T1AM (FL-T1AM) by conjugating it to rhodamine (TRITC) and analyzed its cel
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2

Saba, Alessandro, Grazia Chiellini, Sabina Frascarelli, et al. "Tissue Distribution and Cardiac Metabolism of 3-Iodothyronamine." Endocrinology 151, no. 10 (2010): 5063–73. http://dx.doi.org/10.1210/en.2010-0491.

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3-Iodothyronamine (T1AM) is a novel relative of thyroid hormone, able to interact with specific G protein-coupled receptors, known as trace amine-associated receptors. Significant functional effects are produced by exogenous T1AM, including a negative inotropic and chronotropic effect in cardiac preparations. This work was aimed at estimating endogenous T1AM concentration in different tissues and determining its cardiac metabolism. A novel HPLC tandem mass spectrometry assay was developed, allowing detection of T1AM, thyronamine, 3-iodothyroacetic acid, and thyroacetic acid. T1AM was detected
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3

Dinter, Juliane, Noushafarin Khajavi, Jessica Mühlhaus та ін. "The Multitarget Ligand 3-Iodothyronamine Modulates β-Adrenergic Receptor 2 Signaling". European Thyroid Journal 4, Suppl. 1 (2015): 21–29. http://dx.doi.org/10.1159/000381801.

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Background: 3-Iodothyronamine (3-T1AM), a signaling molecule with structural similarities to thyroid hormones, induces numerous physiological responses including reversible body temperature decline. One target of 3-T1AM is the trace amine-associated receptor 1 (TAAR1), which is a member of the rhodopsin-like family of G protein-coupled receptors (GPCRs). Interestingly, the effects of 3-T1AM remain detectable in TAAR1 knockout mice, suggesting further targets for 3-T1AM such as adrenergic receptors. Therefore, we evaluated whether β-adrenergic receptor 1 (ADRB1) and 2 (ADRB2) signaling is affec
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4

Ghelardoni, Sandra, Grazia Chiellini, Sabina Frascarelli, Alessandro Saba, and Riccardo Zucchi. "Uptake and metabolic effects of 3-iodothyronamine in hepatocytes." Journal of Endocrinology 221, no. 1 (2014): 101–10. http://dx.doi.org/10.1530/joe-13-0311.

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3-Iodothyronamine (T1AM) is an endogenous relative of thyroid hormone with profound metabolic effects. In different experimental models, T1AM increased blood glucose, and it is not clear whether this effect is entirely accounted by changes in insulin and/or glucagone secretion. Thus, in the present work, we investigated the uptake of T1AM by hepatocytes, which was compared with the uptake of thyroid hormones, and the effects of T1AM on hepatic glucose and ketone body production. Two different experimental models were used: HepG2 cells and perfused rat liver. Thyronines and thyronamines (T0AMs)
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5

Dinter, Juliane, Jessica Mühlhaus, Simon Friedrich Jacobi та ін. "3-iodothyronamine differentially modulates α-2A-adrenergic receptor-mediated signaling". Journal of Molecular Endocrinology 54, № 3 (2015): 205–16. http://dx.doi.org/10.1530/jme-15-0003.

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Mostin vivoeffects of 3-iodothyronamine (3-T1AM) have been thus far thought to be mediated by binding at the trace amine-associated receptor 1 (TAAR1). Inconsistently, the 3-T1AM-induced hypothermic effect still persists inTaar1knockout mice, which suggests additional receptor targets. In support of this general assumption, it has previously been reported that 3-T1AM also binds to the α-2A-adrenergic receptor (ADRA2A), which modulates insulin secretion. However, the mechanism of this effect remains unclear. We tested two different scenarios that may explain the effect: the sole action of 3-T1A
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6

Haiyan, Zhou, Hu Bailong, Zhang Bei, Wang Yiming, and Liu Xingde. "Comparative Transcriptome Analysis Reveals the Potential Cardiovascular Protective Targets of the Thyroid Hormone Metabolite 3-Iodothyronamine (3-T1AM)." BioMed Research International 2020 (June 20, 2020): 1–10. http://dx.doi.org/10.1155/2020/1302453.

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Background. The thyroid hormone metabolite 3-iodothyronamine (3-T1AM) is rapidly emerging as a promising compound in decreasing the heart rate and lowering the cardiac output. The aim of our study was to fully understand the molecular mechanism of 3-T1AM on cardiomyocytes and its potential targets in cardiovascular diseases. Materials and Methods. In our study, we utilized RNA-Seq to characterize the gene expression in H9C2 cells after 3-T1AM treatment. Comparative transcriptome analysis, including gene ontology, signaling pathways, disease connectivity analysis, and protein-protein interactio
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7

Cöster, Maxi, Heike Biebermann, Torsten Schöneberg, and Claudia Stäubert. "Evolutionary Conservation of 3-Iodothyronamine as an Agonist at the Trace Amine-Associated Receptor 1." European Thyroid Journal 4, Suppl. 1 (2015): 9–20. http://dx.doi.org/10.1159/000430839.

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Objectives: The trace amine-associated receptor 1 (Taar1) is a Gs protein-coupled receptor activated by trace amines, such as β-phenylethylamine (β-PEA) and 3-iodothyronamine (T1AM). T1AM is an endogenous biogenic amine and thyroid hormone derivative that exerts several biological functions. However, the physiological relevance of T1AM acting via Taar1 is still under discussion. Therefore, we studied the structural and functional evolution of Taar1 in vertebrates to provide evidence for a conserved Taar1-mediated T1AM function. Study Design: We searched public sequence databases to retrieve Ta
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8

Gencarelli, Manuela, Annunziatina Laurino, Elisa Landucci, et al. "3-Iodothyronamine Affects Thermogenic Substrates’ Mobilization in Brown Adipocytes." Biology 9, no. 5 (2020): 95. http://dx.doi.org/10.3390/biology9050095.

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We investigated the effect of 3-iodothyronamine (T1AM) on thermogenic substrates in brown adipocytes (BAs). BAs isolated from the stromal fraction of rat brown adipose tissue were exposed to an adipogenic medium containing insulin in the absence (M) or in the presence of 20 nM T1AM (M+T1AM) for 6 days. At the end of the treatment, the expression of p-PKA/PKA, p-AKT/AKT, p-AMPK/AMPK, p-CREB/CREB, p-P38/P38, type 1 and 3 beta adrenergic receptors (β1–β3AR), GLUT4, type 2 deiodinase (DIO2), and uncoupling protein 1 (UCP-1) were evaluated. The effects of cell conditioning with T1AM on fatty acid m
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9

Galli, Elena, Maja Marchini, Alessandro Saba, et al. "Detection of 3-Iodothyronamine in Human Patients: A Preliminary Study." Journal of Clinical Endocrinology & Metabolism 97, no. 1 (2012): E69—E74. http://dx.doi.org/10.1210/jc.2011-1115.

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Context and Objective: The primary purpose of this study was to detect and quantify 3-iodothyronamine (T1AM), an endogenous biogenic amine related to thyroid hormone, in human blood. Design: T1AM, total T3, and total T4 were assayed in serum by a novel HPLC tandem mass spectrometry assay, which has already been validated in animal investigations, and the results were related to standard clinical and laboratory variables. Setting and Patients: The series included one healthy volunteer, 24 patients admitted to a cardiological ward, and 17 ambulatory patients suspected of thyroid disease, who und
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10

Hackenmueller, Sarah A., Maja Marchini, Alessandro Saba, Riccardo Zucchi, and Thomas S. Scanlan. "Biosynthesis of 3-Iodothyronamine (T1AM) Is Dependent on the Sodium-Iodide Symporter and Thyroperoxidase but Does Not Involve Extrathyroidal Metabolism of T4." Endocrinology 153, no. 11 (2012): 5659–67. http://dx.doi.org/10.1210/en.2012-1254.

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Abstract 3-Iodothyronamine (T1AM) is an endogenous thyroid hormone derivative with unknown biosynthetic origins. Structural similarities have led to the hypothesis that T1AM is an extrathyroidal metabolite of T4. This study uses an isotope-labeled T4 [heavy-T4 (H-T4)] that can be distinguished from endogenous T4 by mass spectrometry, which allows metabolites to be identified based on the presence of this unique isotope signature. Endogenous T1AM levels depend upon thyroid status and decrease upon induction of hypothyroidism. However, in hypothyroid mice replaced with H-T4, the isotope-labeled
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