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Relevant bibliographies by topics / 5-diiodo-L-thyronine

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Academic literature on the topic '5-diiodo-L-thyronine'

Author: Grafiati

Published: 14 March 2023

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Journal articles on the topic "5-diiodo-L-thyronine"

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Markova, Natalyia, Anton Chernopiatko, Careen A. Schroeter, et al. "Hippocampal Gene Expression of Deiodinases 2 and 3 and Effects of 3,5-Diiodo-L-Thyronine T2 in Mouse Depression Paradigms." BioMed Research International 2013 (2013): 1–14. http://dx.doi.org/10.1155/2013/565218.

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Central thyroid hormone signaling is important in brain function/dysfunction, including affective disorders and depression. In contrast to 3,3′,5-triiodo-L-thyronine (T3), the role of 3,5-diiodo-L-thyronine (T2), which until recently was considered an inactive metabolite of T3, has not been studied in these pathologies. However, both T3 and T2 stimulate mitochondrial respiration, a factor counteracting the pathogenesis of depressive disorder, but the cellular origins in the CNS, mechanisms, and kinetics of the cellular action for these two hormones are distinct and independent of each other. H

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Scapin, Sergio, Silvia Leoni, Silvana Spagnuolo, Anna Maria Fiore, and Sandra Incerpi. "Short-term effects of thyroid hormones on Na+-K+-ATPase activity of chick embryo hepatocytes during development: focus on signal transduction." American Journal of Physiology-Cell Physiology 296, no. 1 (2009): C4—C12. http://dx.doi.org/10.1152/ajpcell.90604.2007.

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Nongenomic effects of thyroid hormones on Na+-K+-ATPase activity were studied in chick embryo hepatocytes at two different developmental stages, 14 and 19 days of embryonal age, and the signal transduction pathways involved were characterized. Our data showed the following. 1) 3,5,3′-Triiodo-l-thyronine (T3) and 3,5-diiodo-l-thyronine (3,5-T2) rapidly induced a transient inhibitory effect on the Na+-K+-ATPase; the extent and duration depended on the developmental age of the cells. 2) 3,5-T2 behaved as a true hormone and fully mimicked the effect of T3. 3) Thyroxine had no effect at any of the

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Baur, A., K. Bauer, H. Jarry, and J. Köhrle. "3,5-Diiodo-l-Thyronine Stimulates Type 1 5′Deiodinase Activity in Rat Anterior Pituitariesin Vivoand in Reaggregate Cultures and GH3 Cellsin Vitro1." Endocrinology 138, no. 8 (1997): 3242–48. http://dx.doi.org/10.1210/endo.138.8.5333.

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Del Viscovo, Adelaide, Agnese Secondo, Alba Esposito, Fernando Goglia, Maria Moreno, and Lorella M. T. Canzoniero. "Intracellular and plasma membrane-initiated pathways involved in the [Ca2+]i elevations induced by iodothyronines (T3 and T2) in pituitary GH3 cells." American Journal of Physiology-Endocrinology and Metabolism 302, no. 11 (2012): E1419—E1430. http://dx.doi.org/10.1152/ajpendo.00389.2011.

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The role of 3,5,3′-triiodo-l-thyronine (T3) and its metabolite 3,5-diiodo-l-thyronine (T2) in modulating the intracellular Ca2+ concentration ([Ca2+]i) and endogenous nitric oxide (NO) synthesis was evaluated in pituitary GH3 cells in the absence or presence of extracellular Ca2+. When applied in Ca2+-free solution, T2 and T3 increased [Ca2+]i, in a dose-dependent way, and NO levels. Inhibition of neuronal NO synthase by NG-nitro-l-arginine methyl ester and l- n5-(1-iminoethyl)ornithine hydrochloride significantly reduced the [Ca2+]i increase induced by T2 and T3. However, while depletion of i

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Dissertations / Theses on the topic "5-diiodo-L-thyronine"

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Lehmphul, Ina. "Zelluläre Wirkung, Wirkmechanismen und Nachweisverfahren von Schilddrüsenhormonen und ihren Metaboliten." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2015. http://dx.doi.org/10.18452/17434.

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Schilddrüsenhormone (TH) regulieren Metabolismus und Energiestoffwechsel. Der TH‐Metabolit (THM) 3,5‐T2 (3,5‐Diiod‐L‐Thyronin) aktiviert Fett‐Oxidation und mitochondriale Atmung. Der THM 3‐Iodothyronamin (3‐T1AM) beeinflusst zusätzlich glukoregulatorische Prozesse. THM können zur Reduktion von Körperfett beitragen. Um 3,5‐T2 im humanen Serum nachzuweisen sollte ein Immunoassay aufgebaut, validiert und angewendet werden. In intakten hepatozellulären (HepG2) sowie pankreatischen ß‐Zellen (MIN6) sollte untersucht werden ob THM durch Modulation der mitochondrialen Aktivität die zelluläre Substra

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