Увійти

Готові списки джерел за темами / Thyronine / Статті в журналах

Статті в журналах з теми "Thyronine"

Щоб переглянути інші типи публікацій з цієї теми, перейдіть за посиланням: Thyronine.

Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 28 січня 2023

Оформте джерело за APA, MLA, Chicago, Harvard та іншими стилями

Оберіть тип джерела:

Ознайомтеся з топ-50 статей у журналах для дослідження на тему "Thyronine".

Біля кожної праці в переліку літератури доступна кнопка «Додати до бібліографії». Скористайтеся нею – і ми автоматично оформимо бібліографічне посилання на обрану працю в потрібному вам стилі цитування: APA, MLA, «Гарвард», «Чикаго», «Ванкувер» тощо.

Також ви можете завантажити повний текст наукової публікації у форматі «.pdf» та прочитати онлайн анотацію до роботи, якщо відповідні параметри наявні в метаданих.

Переглядайте статті в журналах для різних дисциплін та оформлюйте правильно вашу бібліографію.

1

Witherspoon, L. R., A. S. el Shami, S. E. Shuler, H. Neely, R. Sonnemaker, S. S. Gilbert, and K. Alyea. "Chemically blocked analog assays for free thyronines. II. Use of equilibrium dialysis to optimize the displacement by chemical blockers of T4 analog and T3 analog from albumin while avoiding displacement of T4 and T3 from thyroxin-binding globulin." Clinical Chemistry 34, no. 1 (January 1, 1988): 17–23. http://dx.doi.org/10.1093/clinchem/34.1.17.

Повний текст джерела

Анотація:

Abstract Chemical blockers used to displace thyronine analog from albumin in analog kits for assay of free thyroxin (FT4) or free triiodothyronine (FT3) may also displace thyroxin (T4) or triiodothyronine (T3) from thyroxin-binding globulin (TBG), resulting in an apparent TBG dependence of results of free hormone estimates. We used equilibrium dialysis and antibody binding to assess the displacement of thyronine analogs and thyronines from albumin and TBG by use of chemical blockers. We chose a combination of two chemical blockers, which eliminated thyronine analog-albumin binding but minimized thyronine displacement from TBG for use in FT4 and FT3 assays. These blocked-analog free-hormone assays yielded accurate clinical results in euthyroid patients, hypo- and hyperthyroid patients, and in pregnant women. FT4 results were not entirely normalized in all nonthyroidally ill patients, indicating that decreased analog-albumin binding is not the only factor resulting in low FT4 results. In current Diagnostic Products Corp. (DPC) FT4 and FT3 blocked-analog kits, the blocker concentrations are the same as we used in these assays.

Стилі APA, Harvard, Vancouver, ISO та ін.

2

Zhu, Fan-Fan, and Li-Zhen Yang. "The Association Between the Levels of Thyroid Hormones and Peripheral Nerve Conduction in Patients with Type 2 Diabetes Mellitus." Experimental and Clinical Endocrinology & Diabetes 126, no. 08 (June 26, 2018): 493–504. http://dx.doi.org/10.1055/a-0635-0826.

Повний текст джерела

Анотація:

Abstract Background Type 2 diabetes has an underlying pathology with thyroid dysfunction. However, few studies have investigated the association between thyroid hormones and diabetic peripheral neuropathy. Our aim was to evaluate the relationship between thyroid hormones and electrophysiological properties of peripheral nerves in type 2 diabetes. Patients and Methods The medical records of 308 patients with type 2 diabetes were enrolled in this study. Subjects stratified by sex were divided into subgroups based on the diagnosis of nerve conduction study. The nerve conduction parameters were separately described with the spectrum of thyroid hormones. Multivariate regression models to analyze the potential links between thyroid hormones and nerve conduction parameters. Results The serum free triiodine thyronine levels between normal and abnormal nerve conduction groups were statistically different in total (4.55±0.65 vs 4.37±0.63, P<0.05) and female diabetic patients (4.46±0.50 vs 4.14±0.57, P<0.01). Moreover, the summed amplitude and velocity Z score of female and male increased with free triiodine thyronine levels (P<0.05). Sex-specific binary logistic regression models showed that free triiodine thyronine levels were associated with decreased odds of abnormal nerve conduction diagnosis (odds ratio [95%CI]=0.151[0.047-0.186]) and low tertile of summed amplitude Z score (odds ratio [95%CI]=0.283[0.099-0.809]) in female. In total patients, free triiodine thyronine level was negatively associated with odds of abnormal nerve conduction (odds ratio [95%CI]=0.436 [0.226-0.842]), low tertile of summed velocity (odds ratio [95%CI]=0.44[0.226-0.858]) and amplitude (odds ratio [95%CI]=0.436[0.227-0.838) Z score. Conclusions Serum free triiodine thyronine level is associated with nerve conduction in diabetes. Low free triiodine thyronine may be a potential risk for diabetic peripheral neuropathy.

Стилі APA, Harvard, Vancouver, ISO та ін.

3

Aceves, C., and R. Rojas-Huidobro. "Effect of suckling and adrenergic stimulation on peripheral deiodination in lactating rats: differential expression of type 1 deiodinase mRNA forms." Journal of Endocrinology 171, no. 3 (December 1, 2001): 533–40. http://dx.doi.org/10.1677/joe.0.1710533.

Повний текст джерела

Анотація:

Previous works led us to propose that peripheral iodothyronine deiodination is mainly regulated by the reciprocal interaction between the thyroid and the sympathetic nervous system (SNS). In this study, we analyzed the role suckling exerts, through SNS activation, upon deiodination of thyronines in liver, heart, brown adipose tissue and mammary gland during lactation. Our results showed that resuckling causes a concurrent stimulatory response on deiodinase type 1 (D1) in heart and mammary gland, but not in liver and brown adipose tissue. The stimulatory response was mimicked by norepinephrine and by the beta-adrenergic agonist isoproterenol, through the overexpression of the large form of D1 mRNA. These results suggested that, during lactation, peripheral thyronine deiodination is co-ordinated by the SNS, and suckling is a major modulatory influence.

Стилі APA, Harvard, Vancouver, ISO та ін.

4

Valashek, I. E., P. M. Kochergin, E. M. Vinogradova, and L. I. Budanova. "Synthesis of 3,5-Diiodo-DL-thyronine." Pharmaceutical Chemistry Journal 29, no. 6 (June 1995): 418–19. http://dx.doi.org/10.1007/bf02220547.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

5

SHOJAEE-MORADIE, Fariba, Michelle P. Y. CHAN, Micayla A. TELFER, Dietrich BRANDENBURG, Erik SUNDERMANN, Heike ECKEY, Jens KLEINJUNG, Achim SCHÜTTLER, and Richard H. JONES. "Effect of thyroid hormone binding proteins on insulin receptor binding of B1-thyronine-insulin analogues." Biochemical Journal 381, no. 1 (June 22, 2004): 51–57. http://dx.doi.org/10.1042/bj20040177.

Повний текст джерела

Анотація:

Certain thyronine-insulin analogues, which form non-covalent complexes with plasma proteins, have been shown to act preferentially in the liver. We hypothesized that this property may be dependant on the ability of the analogue to bind to the insulin receptor without prior dissociation from the binding protein. NαB1-L-thyroxyl-insulin, NαB1-3,3′,5′-triiodothyronine-insulin, NαB1-D-thyroxyl-insulin and NαB1-L-thyroxyl-aminolauroyl-insulin were compared with insulin for their capacity to inhibit the binding of [125I]TyrA14-insulin to rat liver plasma membrane in albumin-free buffer. Effective doses at 50% maximum inhibition of binding (ED50) were calculated with and without addition of the thyroid hormone binding proteins transthyretin, thyroxine binding globulin and human serum albumin. The binding of thyronine-insulin analogues to insulin receptors was inhibited in a dose-dependant manner by the addition of thyroid hormone binding proteins at concentrations in the physiological range. Complexes of thyronine-insulin analogues with thyroid hormone binding proteins exhibit impaired insulin receptor binding affinities compared with those of the analogues in their free form. Hepatoselectivity in vivo may not depend on binding of the intact complexes to hepatocytes. These results have implications for the physiological role of hormone binding proteins and the in vivo properties of other insulin analogues which bind to plasma proteins.

Стилі APA, Harvard, Vancouver, ISO та ін.

6

Oziol, L., P. Faure, N. Bertrand, and P. Chomard. "Inhibition of in vitro macrophage-induced low density lipoprotein oxidation by thyroid compounds." Journal of Endocrinology 177, no. 1 (April 1, 2003): 137–46. http://dx.doi.org/10.1677/joe.0.1770137.

Повний текст джерела

Анотація:

Oxidized low density lipoproteins (LDL) are highly suspected of initiating the atherosclerosis process. Thyroid hormones and structural analogues have been reported to protect LDL from lipid peroxidation induced by Cu2+ or the free radical generator 2,2'-azobis-'2-amidinopropane' dihydrochloride in vitro. We have examined the effects of thyroid compounds on macrophage-induced LDL oxidation. Human monocyte-derived macrophages (differentiated U937 cells) were incubated for 24 h with LDL and different concentrations (0-20 microM) of 3,5,3'-triiodo-l -thyronine (T3), 3,5,3',5'-tetraiodo-L-thyronine (T4), 3,3',5'-tri-iodo-l -thyronine (rT3), the T3 acetic derivative (3,5,3'-tri-iodothyroacetic acid; TA3) or L-thyronine (T0) (experiment 1). Cells were also preincubated for 24 h with 1 or 10 microM of the compounds, washed twice, then incubated again for 24 h with LDL (experiment 2). Oxidation was evaluated by measurement of thiobarbituric acid-reactive substances (TBARS) and cell viability by lactate deshydrogenase release. In experiment 1, T0 had no effect, whereas the other compounds decreased LDL TBARS production, but T3 and TA3 were less active than T4 and rT3 (IC50: 11.0 +/- 2.6 and 8.1 +/- 0.8 vs 1.4 +/- 0.5 and 0.9 +/- 0.3 microM respectively). In experiment 2, the compounds at 1 microM had no effect; at 10 microM, T3 and rT3 slightly reduced LDL TBARS production, whereas TA3 and T4 inhibited it by about 50% and 70% respectively. TBARS released by the cells were also highly decreased by T3, T4, rT3 and TA3 in experiment 1, but only by T3 (30%) and T4 (70%) in experiment 2. Cell viability was not affected by the compounds except slightly by TA3 at 10 microM. The data suggested that the physico-chemical antioxidant capacity of thyroid compounds was modulated by their action on the intracellular redox systems of macrophage. Overall cellular effects of T3 led to a reduction of its antioxidant capacity whereas those of T4 increased it. Thus T4 might protect LDL against cellular oxidation in vivo more than T3.

Стилі APA, Harvard, Vancouver, ISO та ін.

7

Segal, J., J. Hardiman, and S. H. Ingbar. "Stimulation of calcium-ATPase activity by 3,5,3′-tri-iodothyronine in rat thymocyte plasma membranes. A possible role in the modulation of cellular calcium concentration." Biochemical Journal 261, no. 3 (August 1, 1989): 749–54. http://dx.doi.org/10.1042/bj2610749.

Повний текст джерела

Анотація:

We have previously demonstrated that 3,5,3′-tri-iodo-L-thyronine (T3) produces a very rapid and transient increase in calcium uptake and cytoplasmic free calcium concentration in the rat thymocyte, and have postulated that Ca2+-ATPase may contribute to the overall effect of T3 on cellular calcium metabolism. In the present study, we show that in the rat thymocyte, T3 increased plasma membrane Ca2+-ATPase activity. This effect of T3 was very rapid, seen at 30 s after the addition of the hormone, and was concentration-related, evident at a physiological concentration as low as 1 pM. Evaluation of the effect of several thyronine analogues on Ca2+-ATPase activity revealed the following order of potency: D-T3 greater than or equal to 3′-isopropyl-L-T2 = L-T3 = L-T4 = D-T4 greater than L-rT3 greater than 3,5-L-T2 greater than DL-thyronine. Studies with the calmodulin antagonist trifluoperazine demonstrated that thymocyte Ca2+-ATPase activity and its stimulation by T3 are influenced by calmodulin. Other studies showed that several adrenergic agents, agonists and antagonists, had no effect on thymocyte Ca2+-ATPase activity and its stimulation by T3. From these and previous observations, we would suggest that in the rat thymocyte, the T3-induced increase in Ca2+-ATPase activity, which enhances the expulsion of calcium from the cell, plays a role in the diminution and transiency of the stimulatory effect of T3 on thymocyte calcium metabolism.

Стилі APA, Harvard, Vancouver, ISO та ін.

8

Coppola, Maria, Federica Cioffi, Maria Moreno, Fernando Goglia, and Elena Silvestri. "3,5-diiodo-L-thyronine: A Possible Pharmacological Agent?" Current Drug Delivery 13, no. 3 (May 20, 2016): 330–38. http://dx.doi.org/10.2174/1567201813666151123124340.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

9

Li, Shanshan, Bing Yang, Tomonori Kobayashi, Bingchen Yu, Jun Liu, and Lei Wang. "Genetically encoding thyronine for fluorescent detection of peroxynitrite." Bioorganic & Medicinal Chemistry 28, no. 18 (September 2020): 115665. http://dx.doi.org/10.1016/j.bmc.2020.115665.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

10

VALASHEK, I. E., P. M. KOCHERGIN, E. M. VINOGRADOVA, and L. I. BUDANOVA. "ChemInform Abstract: Synthesis of 3,5-Diiodo-DL-thyronine." ChemInform 27, no. 2 (August 12, 2010): no. http://dx.doi.org/10.1002/chin.199602253.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

11

Oziol, L., P. Faure, C. Vergely, L. Rochette, Y. Artur, P. Chomard, and P. Chomard. "In vitro free radical scavenging capacity of thyroid hormones and structural analogues." Journal of Endocrinology 170, no. 1 (July 1, 2001): 197–206. http://dx.doi.org/10.1677/joe.0.1700197.

Повний текст джерела

Анотація:

It was reported that thyroid hormones decreased Cu(2+)-induced low-density lipoprotein (LDL) oxidation in vitro. Here, we investigated free radical scavenging capacities of thyroid hormones (3,5,3'-tri-iodo-L-thyronine (T(3)), thyroxine (T(4)) and 3,3',5'-tri-iodo-L-thyronine (rT(3))) and structural analogues (L-thyronine (T(0)), 3,5,3'tri-iodothyroacetic acid (TA(3)) and 3,5,3',5'-tetra-iodothyroacetic acid (TA(4))), using three different models of free radical generation. T(0), T(3) and TA(3) slowed down production of conjugated diene and thiobarbituric acid-reactive substances during LDL oxidation by 2,2'-azobis-[2-amidinopropane] (water-soluble), whereas rT(3), T(4) and TA(4) had practically no effect. In this system, T(0) was the more active compound. Using a 1,1-diphenyl-2-picrylhydrazyl (lipid-soluble) test, all compounds also revealed free radical scavenging capacities, but rT(3), T(4) and TA(4) were more active than T(0), T(3) and TA(3). T(3) was able to scavenge superoxide anion and hydroxyl radicals generated in an aqueous phase by a xanthine-xanthine oxidase system, as measured by electron paramagnetic resonance spectroscopy. It may be concluded that: (1) thyroid hormones and analogues with a 4'-hydroxy diphenylether structure have free radical scavenging capacities, (2) this property is influenced by the number of iodines on the phenolic ring, and (3) thyroid hormone scavenging capacity should not be the only mechanism explaining their protective effect on Cu(2+)-induced LDL oxidation. The physiological significance of the findings is discussed.

Стилі APA, Harvard, Vancouver, ISO та ін.

12

Silvestri, Elena, Assunta Lombardi, Maria Coppola, Alessandra Gentile, Federica Cioffi, Rosalba Senese, Fernando Goglia, Antonia Lanni, Maria Moreno, and Pieter de Lange. "Differential Effects of 3,5-Diiodo-L-Thyronine and 3,5,3’-Triiodo-L-Thyronine On Mitochondrial Respiratory Pathways in Liver from Hypothyroid Rats." Cellular Physiology and Biochemistry 47, no. 6 (2018): 2471–83. http://dx.doi.org/10.1159/000491620.

Повний текст джерела

Анотація:

Background/Aims: Both 3,5-diiodo-L-thyronine (3,5-T2) and 3,5,3’-triiodo-L-tyronine (T3) affect energy metabolism having mitochondria as a major target. However, the underlying mechanisms are poorly understood. Here, using a model of chemically induced hypothyroidism in male Wistar rats, we investigated the effect of administration of either 3,5-T2 or T3 on liver oxidative capacity through their influence on mitochondrial processes including: proton-leak across the mitochondrial inner membrane; complex I-, complex II- and glycerol-3-phosphate-linked respiratory pathways; respiratory complex abundance and activities as well as individual complex aggregation into supercomplexes. Methods: Hypothyroidism was induced by propylthiouracil and iopanoic acid; 3,5-T2 and T3 were intraperitoneally administered at 25 and 15 µg/100 g BW for 1 week, respectively. Resulting alterations in mitochondrial function were studied by combining respirometry, Blue Native-PAGE followed by in-gel activity, and Western blot analyses. Results: Administration of 3,5-T2 and T3 to hypothyroid (hypo) rats enhanced mitochondrial respiration rate with only T3 effectively stimulating proton-leak (450% vs. Hypo). T3 significantly enhanced complex I (+145% vs. Hypo), complex II (+66% vs. Hypo), and glycerol-3 phosphate dehydrogenase (G3PDH)-linked oxygen consumptions (about 6- fold those obtained in Hypo), while 3,5-T2 administration selectively restored Euthyroid values of complex II- and increased G3PDH- linked respiratory pathways (+165% vs. Hypo). The mitochondrial abundance of all respiratory complexes and of G3PDH was increased by T3 administration whereas 3,5-T2 only increased complex V and G3PDH abundance. 3,5-T2 enhanced complex I and complex II in gel activities with less intensity than did T3, and T3 also enhanced the activity of all other respiratory complexes tested. In addition, only T3 enhanced individual respiratory component complex assembly into supercomplexes. Conclusions: The reported data highlight novel molecular mechanisms underlying the effect elicited by iodothyronine administration to hypothyroid rats on mitochondrial processes related to alteration in oxidative capacity in the liver. The differential effects elicited by the two iodothyronines indicate that 3,5-T2, by influencing the kinetic properties of specific mitochondrial respiratory pathways, would promote a rapid response of the organelle, while T3, by enhancing the abundance of respiratory chain component and favoring the organization of respiratory chain complex in supercomplexes, would induce a slower and prolonged response of the organelle.

Стилі APA, Harvard, Vancouver, ISO та ін.

13

Vacek, Jan, Pavel Kosina, Eva Gabrielová, Martin Modrianský, and Jitka Ulrichová. "Ion-trap mass spectrometry for determination of 3,5,3′-triiodo-l-thyronine and 3,5,3′,5′-tetraiodo-l-thyronine in neonatal rat cardiomyocytes." Journal of Pharmaceutical and Biomedical Analysis 53, no. 3 (November 2010): 688–92. http://dx.doi.org/10.1016/j.jpba.2010.03.018.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

14

Lanni, A., M. Moreno, A. Lombardi, and F. Goglia. "Rapid stimulation in vitro of rat liver cytochrome oxidase activity by 3,5-diiodo-l-thyronine and by 3,3′-diiodo-l-thyronine." Molecular and Cellular Endocrinology 99, no. 1 (February 1994): 89–94. http://dx.doi.org/10.1016/0303-7207(94)90150-3.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

15

Ouyang, Jingping. "Triiodo-thyronine reverses angiotensin induced cardiomyocyte b-mhc expression." Canadian Journal of Anesthesia/Journal canadien d'anesthésie 53, no. 1 (January 2006): 26402. http://dx.doi.org/10.1007/bf03017008.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

16

Lanni, Antonia, Maria Moreno, Assunta Lombardi, and F. Goglia. "3,5-Diiodo- l -thyronine and 3,5,3′-triiodo- l -thyronine both improve the cold tolerance of hypothyroid rats, but possibly via different mechanisms." Pfl�gers Archiv European Journal of Physiology 436, no. 3 (June 29, 1998): 407–14. http://dx.doi.org/10.1007/s004240050650.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

17

Aboul-Enein, Hassan Y., Stefan Raluca-Ioana, Simona Litescu, and Gabriel Lucian Radu. "BIOSENSOR FOR THE ENANTIOSELECTIVE ANALYSIS OF THE THYROID HORMONES (+)-3,3′,5-TRIIODO-L-THYRONINE (T3) AND (+)-3,3′,5,5′-TETRAIODO-L-THYRONINE (T4)." Journal of Immunoassay and Immunochemistry 23, no. 2 (May 15, 2002): 181–90. http://dx.doi.org/10.1081/ias-120003660.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

18

Beslin, A., M. P. Vié, J. P. Blondeau, and J. Francon. "Identification by photoaffinity labelling of a pyridine nucleotide-dependent tri-iodothyronine-binding protein in the cytosol of cultured astroglial cells." Biochemical Journal 305, no. 3 (February 1, 1995): 729–37. http://dx.doi.org/10.1042/bj3050729.

Повний текст джерела

Анотація:

High-affinity 3,3′,5-tri-iodo-L-thyronine (T3) binding (Kd approximately 0.3 nM) to the cytosol of cultured rat astroglial cells was strongly activated in the presence of pyridine nucleotides. A 35 kDa pyridine nucleotide-dependent T3-binding polypeptide (35K-TBP) was photoaffinity labelled using underivatized [125I]T3 in the presence of pyridine nucleotides and the free-radical scavenger dithiothreitol. Maximum activations of T3 binding and 35K-TBP photolabelling were obtained at approx. 1 x 10(-7) M NADP+ or NADPH, or 1 x 10(-4) M NADH. NAD+ and other nucleotides were without effect. NADPH is the form which activates T3 binding and 35K-TBP photolabelling, since cytosol contains NADP(+)-reducing activity, and the activation of both processes in the presence of NADPH and NADP+ was prevented by an exogenous NADPH oxidation system. NADPH behaved as an allosteric activator of T3 binding. The NADPH oxidation system promoted the release of bound T3 in the absence of any change in the total concentration of the hormone. The 35K-TBP photolabelling and [125I]T3 binding were similarly inhibited by non-radioactive T3 (half-maximum effect at 0.5-1.0 nM T3). The concentrations of iodothyronine analogues that inhibited both processes were correlated (3,3′,5-tri-iodo-D-thyronine > or = T3 > L-thyroxine > tri-iodothyroacetic acid > 3,3′5′-tri-iodo-L-thyronine). Molecular sieving and density-gradient centrifugation of cytosol identified a 65 kDa T3-binding entity, which included the 35K-TBP. These results indicate that 35K-TBP is the cytosolic entity involved in the pyridine nucleotide-dependent T3 binding, and suggest that the sequestration and release of intracellular thyroid hormones are regulated by the redox state of astroglial cell compartment(s).

Стилі APA, Harvard, Vancouver, ISO та ін.

19

Monk, Julie A., Natalie A. Sims, Katarzyna M. Dziegielewska, Roy E. Weiss, Robert G. Ramsay, and Samantha J. Richardson. "Delayed development of specific thyroid hormone-regulated events in transthyretin null mice." American Journal of Physiology-Endocrinology and Metabolism 304, no. 1 (January 1, 2013): E23—E31. http://dx.doi.org/10.1152/ajpendo.00216.2012.

Повний текст джерела

Анотація:

Thyroid hormones (THs) are vital for normal postnatal development. Extracellular TH distributor proteins create an intravascular reservoir of THs. Transthyretin (TTR) is a TH distributor protein in the circulatory system and is the only TH distributor protein synthesized in the central nervous system. We investigated the phenotype of TTR null mice during development. Total and free 3′,5′,3,5-tetraiodo-l-thyronine (T4) and free 3′,3,5-triiodo-l-thyronine (T3) in plasma were significantly reduced in 14-day-old (P14) TTR null mice. TTR null mice also displayed a delayed suckling-to-weaning transition, decreased muscle mass, delayed growth, and retarded longitudinal bone growth. In addition, ileums from postnatal day 0 (P0) TTR null mice displayed disordered architecture and contained fewer goblet cells than wild type. Protein concentrations in cerebrospinal fluid from P0 and P14 TTR null mice were higher than in age-matched wild-type mice. In contrast to the current literature based on analyses of adult TTR null mice, our results demonstrate that TTR has an important and nonredundant role in influencing the development of several organs.

Стилі APA, Harvard, Vancouver, ISO та ін.

20

Ball, SG, J. Sokolov, and WW Chin. "3,5-Diiodo-L-thyronine (T2) has selective thyromimetic effects in vivo and in vitro." Journal of Molecular Endocrinology 19, no. 2 (October 1, 1997): 137–47. http://dx.doi.org/10.1677/jme.0.0190137.

Повний текст джерела

Анотація:

Recent data have suggested that the iodothyronine, 3,5-diiodo-l-thyronine (T2), has selective thyromimetic activity. In vivo, T2 has been shown to suppress TSH levels at doses that do not produce significant peripheral manifestations of thyroid hormone activity. Furthermore, T2 has been shown to produce smaller increments in peripheral indices of thyroid status than does T3, when doses resulting in equivalent suppression of circulating TSH are compared. We have assessed the selective thyromimetic activity of T2 in vivo and in vitro, and performed in vitro studies to assess the potential molecular basis for these selective properties. T2 was 100-fold less potent than T3 in stimulating GH mRNA levels in GH3 cells. In contrast, the iodothyronines were almost equivalent in their ability to downregulate TRbeta2 mRNA levels in this cell line. Both 3,3'-diiodo-L-thyronine and thyronine exhibited no significant thyromimetic effects on either process. In vivo, doses of T2 and T3 that were equivalent in their induction of hepatic malic enzyme (ME) mRNA did not produce equivalent suppression of circulating TSH, with T2 being only 27% as effective as T3. T2 was up to 500-fold less potent than T3 in displacing [125I]-T3 from in vitro translated specific nuclear receptors (TRs) and GH3 cell nuclear extracts. Electrophoretic mobility shift assays, assessing the ability of T2 to produce dissociation of TRbeta1 homodimers from inverted palindrome T3 response elements, indicated that T2 was also 1000-fold less potent than T3 in this respect. These data confirm that T2 has significant thyromimetic activity, and that this activity is selective both in vivo and in vitro. However, there are no data to support a selective central effect, T2 being relatively more potent in stimulating hepatic ME mRNA than in suppression of TSH in vivo. The basis for this differential thyromimetic activity is not selective affinity of the different TR isoforms for T2, or divergent properties of T2 in competitive binding and functional assays in vitro.

Стилі APA, Harvard, Vancouver, ISO та ін.

21

Mano, M. T., B. J. Potter, G. B. Belling, D. M. Martin, B. G. Gragg, J. Chavadej, and B. S. Hetzel. "The effect of thyroxine, 3,5-dimethyl-3'-isopropyl-L-thyronine and iodized oil on fetal brain development in the iodine-deficient sheep." Acta Endocrinologica 121, no. 1 (July 1989): 7–15. http://dx.doi.org/10.1530/acta.0.1210007.

Повний текст джерела

Анотація:

Abstract. Studies have been carried out to investigate the role of maternal and fetal thyroid function in the effects of iodine deficiency on fetal brain development in sheep. Iodine deficiency was established with an especially prepared low-iodine diet of maize and pea pollard. The iodine-deficient sheep were mated and at the end of the second trimester of pregnancy (100 days gestation) were divided into groups which received either a sc injection of T4 or 3,5-dimethyl-3'-isopropyl-L-thyronine or an im injection of iodized oil. At 140 days gestation (10 days prior to parturition) comparison of the fetuses delivered by hysterotomy revealed that the retarded fetal brain development observed in iodine deficiency was greatly improved by T4 and by iodized oil. However, T4 and iodized oil failed to correct the reduction in the number and the increase in the length of synaptic appositions which were observed in the fetal cerebral cortex after iodine deficiency. In addition, the histological appearance of the fetal thyroid gland and the levels of plasma thyroid hormones were restored to normal. The administration of 3,5-dimethyl-3'-isopropyl-L-thyronine had no effect on the retarded fetal brain and body development of the iodine-deficient fetuses. The lack of response may be due to the inability of 3,5-dimethyl-3'-isopropyl-L-thyronine to cross the ovine placenta as no reduction in the abnormally elevated fetal plasma TSH was observed in spite of a fall in maternal plasma TSH and apparent restoration of maternal thyroid function. It is concluded that the retarded fetal brain development observed during iodine deficiency in sheep can be substantially improved by iodized oil or to a lesser extent by T4 administration at 100 days gestation and that this is dependent on the restoration of both maternal and fetal thyroid function which supports previous observations from this laboratory following fetal and maternal thyroidectomy. The persistence of some effects of iodine deficiency on the fetal brain suggests that irreversible damage may have occurred.

Стилі APA, Harvard, Vancouver, ISO та ін.

22

Moreno, Maria, Antonia Giacco, Celia Di Munno, and Fernando Goglia. "Direct and rapid effects of 3,5-diiodo-L-thyronine (T2)." Molecular and Cellular Endocrinology 458 (December 2017): 121–26. http://dx.doi.org/10.1016/j.mce.2017.02.012.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

23

Betley, Stephen, Matthew Peak, and Loranne Agius. "Triiodo-L-thyronine stimulates glycogen synthesis in rat hepatocyte cultures." Molecular and Cellular Biochemistry 120, no. 2 (1993): 151–58. http://dx.doi.org/10.1007/bf00926088.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

24

Goldberg, Ira J., Li-Shin Huang, Lesley A. Huggins, Shuiqing Yu, Prabhakara R. Nagareddy, Thomas S. Scanlan, and Joel R. Ehrenkranz. "Thyroid Hormone Reduces Cholesterol via a Non-LDL Receptor-Mediated Pathway." Endocrinology 153, no. 11 (November 1, 2012): 5143–49. http://dx.doi.org/10.1210/en.2012-1572.

Повний текст джерела

Анотація:

Abstract Although studies in vitro and in hypothyroid animals show that thyroid hormone can, under some circumstances, modulate the actions of low-density lipoprotein (LDL) receptors, the mechanisms responsible for thyroid hormone's lipid-lowering effects are not completely understood. We tested whether LDL receptor (LDLR) expression was required for cholesterol reduction by treating control and LDLR-knockout mice with two forms of thyroid hormone T3 and 3,5-diiodo-l-thyronine. High doses of both 3,5-diiodo-l-thyronine and T3 dramatically reduced circulating total and very low-density lipoprotein/LDL cholesterol (∼70%) and were associated with reduced plasma T4 level. The cholesterol reduction was especially evident in the LDLR-knockout mice. Circulating levels of both apolipoprotein B (apo)B48 and apoB100 were decreased. Surprisingly, this reduction was not associated with increased protein or mRNA expression of the hepatic lipoprotein receptors LDLR-related protein 1 or scavenger receptor-B1. Liver production of apoB was markedly reduced, whereas triglyceride production was increased. Thus, thyroid hormones reduce apoB lipoproteins via a non-LDLR pathway that leads to decreased liver apoB production. This suggests that drugs that operate in a similar manner could be a new therapy for patients with genetic defects in the LDLR.

Стилі APA, Harvard, Vancouver, ISO та ін.

25

Markova, Natalyia, Anton Chernopiatko, Careen A. Schroeter, Dmitry Malin, Aslan Kubatiev, Sergey Bachurin, João Costa-Nunes, Harry M. W. Steinbusch, and Tatyana Strekalova. "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.

Повний текст джерела

Анотація:

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. Here, Illumina and RT PCR assays showed that hippocampal gene expression of deiodinases 2 and 3, enzymes involved in thyroid hormone regulation, is increased in resilience to stress-induced depressive syndrome and after antidepressant treatment in mice that might suggest elevated T2 and T3 turnover in these phenotypes. In a separate experiment, bolus administration of T2 at the doses 750 and 1500 mcg/kg but not 250 mcg/kg in naive mice reduced immobility in a two-day tail suspension test in various settings without changing locomotion or anxiety. This demonstrates an antidepressant-like effect of T2 that could be exploited clinically. In a wider context, the current study suggests important central functions of T2, whose biological role only lately is becoming to be elucidated.

Стилі APA, Harvard, Vancouver, ISO та ін.

26

O'Neill, David E. T., F. Kris Aubrey, David A. Zeldin, Robin N. Michel, and Earl G. Noble. "Slower skeletal muscle phenotypes are critical for constitutive expression of Hsp70 in overloaded rat plantaris muscle." Journal of Applied Physiology 100, no. 3 (March 2006): 981–87. http://dx.doi.org/10.1152/japplphysiol.00831.2005.

Повний текст джерела

Анотація:

Heat shock protein 72 (Hsp70) is constitutively expressed in rat hindlimb muscles, reportedly in proportion to their content of type I myosin heavy chain. This distribution pattern has been suggested to result from the higher recruitment and activity of such muscles and/or a specific relationship between myosin phenotype and Hsp70 content. To differentiate between these possibilities, the fiber-specific distribution of Hsp70 was examined in male Sprague-Dawley rat plantaris under control conditions, following a fast-to-slow phenotypic shift in response to surgically induced overload (O) and in response to O when the phenotypic shift was prevented by 3,5,3′-triiodo-dl-thyronine administration. Constitutive expression of Hsp70 was restricted to type I and IIa fibers in plantaris from control rats, and this fiber-specific pattern of expression was maintained following O of up to 28 days, although Hsp70 content in the O muscle doubled. When O (for 40 days) of the plantaris was combined with 3,5,3′-triiodo-dl-thyronine administration, despite typical hypertrophy in the overloaded plantaris, prevention of the normal phenotypic transformation also blocked the increased expression of Hsp70 observed in euthyroid controls. Collectively, these data suggest that chronic changes in constitutive expression of Hsp70 with altered contractile activity appear critically dependent on fast-to-slow phenotypic remodeling.

Стилі APA, Harvard, Vancouver, ISO та ін.

27

PONTECORVI, ALFREDO, MARK LAKSHMANAN, and JACOB ROBBINS. "Intracellular Transport of 3,5,3′-Triiodo-L-Thyronine in Rat Skeletal Myoblasts*." Endocrinology 121, no. 6 (December 1987): 2145–52. http://dx.doi.org/10.1210/endo-121-6-2145.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

28

Grymuła, K., E. Paczkowska, V. Dziedziejko, M. Baśkiewicz-Masiuk, M. Kawa, B. Baumert, Z. Celewicz, E. Gawrych, and B. Machaliński. "The influence of 3,3',5-triiodo-l-thyronine on human haematopoiesis." Cell Proliferation 40, no. 3 (June 2007): 302–15. http://dx.doi.org/10.1111/j.1365-2184.2007.00435.x.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

29

Cahnmann, Hans J., Edison Goncalves, Yoichiro Ito, Henry M. Fales, and Edward A. Sokoloski. "Synthesis and characterization of N-bromoacetyl-3,3′,5-triiodo-L-thyronine." Journal of Chromatography A 538, no. 1 (January 1991): 165–75. http://dx.doi.org/10.1016/s0021-9673(01)91634-6.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

30

Bazoma Bayili, Ollo Da, Jean Fidèle Bationo, Véronique Panne Coulibaly, Sylvain Ilboudo, Richard Ouedraogo, Jean Bosco Ouedraogo, and Georges Anicet Ouedraogo. "Evaluation of thyroid disorders in cotton growers exposed to pesticides in Satiri department." GSC Biological and Pharmaceutical Sciences 13, no. 1 (October 30, 2020): 179–88. http://dx.doi.org/10.30574/gscbps.2020.13.1.0325.

Повний текст джерела

Анотація:

Cotton farmers are exposed to a variety of pesticide formulations, some of which contain active endocrine disrupting substances. The objective of this study was to investigate the link between pesticide exposure and thyroid disorders in cotton growers. This was a longitudinal prospective study among cotton producers during and after the 2018/2019 cotton season in the Satiri department. Surveys have been conducted on a cohort of 50 producers to collect socio-demographic and professional information on the producers and the pesticides used. A medical examination of the producers followed by blood samples were carried out during and after the cotton season. The thyroid stimulating hormone (TSH), Free tetra- iodo-thyronine (FT4) and Free tri-iodo-thyronine (FT3) biomarkers were measured on the Cobas®6000 automaton. During the cotton campaign, an overall frequency of 12.00% of dysthyroidism, of which 8.00% of hypothyroidism and 4.00% of hyperthyroidism were recorded. After the campaign, 14.00% dysthyroidism was observed, including 8.00% of hypothyroidism and 6.00% of hyperthyroidism. Also, a significant decrease in TSH concentrations; a significant increase in FT4 and a non-significant decrease in FT3 were observed. This study does not establish a specific link between exposure to pesticides and thyroid disorders due to the complexity and cocktail effect of pesticides. Rational use of these products is essential to avoid health effects linked to endocrine disruption.

Стилі APA, Harvard, Vancouver, ISO та ін.

31

Schroeder, Amy, Robyn Jimenez, Briana Young, and Martin L. Privalsky. "The Ability of Thyroid Hormone Receptors to Sense T4 as an Agonist Depends on Receptor Isoform and on Cellular Cofactors." Molecular Endocrinology 28, no. 5 (May 1, 2014): 745–57. http://dx.doi.org/10.1210/me.2013-1335.

Повний текст джерела

Анотація:

Abstract T4 (3,5,3′,5′-tetraiodo-l-thyronine) is classically viewed as a prohormone that must be converted to the T3 (3,5,3′-triiodo-l-thyronine) form for biological activity. We first determined that the ability of reporter genes to respond to T4 and to T3 differed for the different thyroid hormone receptor (TR) isoforms, with TRα1 generally more responsive to T4 than was TRβ1. The response to T4 vs T3 also differed dramatically in different cell types in a manner that could not be attributed to differences in deiodinase activity or in hormone affinity, leading us to examine the role of TR coregulators in this phenomenon. Unexpectedly, several coactivators, such as steroid receptor coactivator-1 (SRC1) and thyroid hormone receptor-associated protein 220 (TRAP220), were recruited to TRα1 nearly equally by T4 as by T3 in vitro, indicating that TRα1 possesses an innate potential to respond efficiently to T4 as an agonist. In contrast, release of corepressors, such as the nuclear receptor coreceptor NCoRω, from TRα1 by T4 was relatively inefficient, requiring considerably higher concentrations of this ligand than did coactivator recruitment. Our results suggest that cells, by altering the repertoire and abundance of corepressors and coactivators expressed, may regulate their ability to respond to T4, raising the possibility that T4 may function directly as a hormone in specific cellular or physiological contexts.

Стилі APA, Harvard, Vancouver, ISO та ін.

32

Hummerich, H., and S. Soboll. "Rapid stimulation of calcium uptake into rat liver by l-tri-iodothyronine." Biochemical Journal 258, no. 2 (March 1, 1989): 363–67. http://dx.doi.org/10.1042/bj2580363.

Повний текст джерела

Анотація:

The short-term effect of L-tri-iodothyronine (T3) on hepatic Ca2+ uptake from perfusate was compared with changes induced by T3 on cellular respiration and glucose output in isolated perfused livers from fasted and fed rats. The same parameters were also studied after the addition of glucagon or vasopressin. T3 (1 microM) induced Ca2+ uptake from the perfusate into the liver within minutes, and the time course was similar to that for stimulation of respiration and gluconeogenesis in livers from fasted rats, and for the stimulation of respiration and glucose output in livers from fed rats. The effects were dose-dependent in the range 1 microM-0.1 nM. Similar changes in the same parameters could be observed with glucagon and vasopressin, but with a completely different time course. Also, the influence of the T3 analogues L-thyroxine (L-T4), 3,5-di-iodo-L-thyronine (L-T2) and 3,3′,5-tri-iodo-D-thyronine (D-T3) on hepatic energy metabolism was examined. Whereas D-T3 had practically no effect, L-T4 and L-T2 caused changes in Ca2+ uptake, O2 consumption and gluconeogenesis in livers from fasted rats similar to those with T3. It is concluded that changes in mitochondrial and cytosolic Ca2+ concentrations are involved in the stimulation of respiration and glucose metabolism observed with T3, glucagon and vasopressin.

Стилі APA, Harvard, Vancouver, ISO та ін.

33

Goglia, Fernando, Elena Silvestri, and Antonia Lanni. "Thyroid Hormones and Mitochondria." Bioscience Reports 22, no. 1 (February 1, 2002): 17–32. http://dx.doi.org/10.1023/a:1016056905347.

Повний текст джерела

Анотація:

Because of their central role in the regulation of energy-transduction, mitochondria, the major site of oxidative processes within the cell, are considered a likely subcellular target for the action that thyroid hormones exert on energy metabolism. However, the mechanism underlying the regulation of basal metabolic rate (BMR) by thyroid hormones still remains unclear. It has been suggested that these hormones might uncouple substrate oxidation from ATP synthesis, but there are no clear-cut data to support this idea. Two iodothyronines have been identified as effectors of the actions of thyroid hormones on energy metabolism: 3',3,5-triiodo-L-thyronine (T3) and 3,5-diiodo-L-thyronine (T2). Both have significant effects on BMR, but their mechanisms of action are not identical. T3 acts on the nucleus to influence the expression of genes involved in the regulation of cellular metabolism and mitochondria function; 3,5-T2, on the other hand, acts by directly influencing the mitochondrial energy-transduction apparatus. A molecular determinant of the effects of T3 could be uncoupling protein-3 (UCP-3), while the cytochrome-c oxidase complex is a possible target for 3,5-T2. In conclusion, it is likely that iodothyronines regulate energy metabolism by both short-term and long-term mechanisms, and that they act in more than one way in affecting mitochondrial functions.

Стилі APA, Harvard, Vancouver, ISO та ін.

34

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 (January 2009): C4—C12. http://dx.doi.org/10.1152/ajpcell.90604.2007.

Повний текст джерела

Анотація:

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 developmental stages. 4) The inhibition of Na+-K+-ATPase was mediated by activation of protein kinase A, protein kinase C, and phosphoinositide 3-kinase, suggesting several modes of modulation of ATPase activity through phosphorylation at different sites. 5) The MAPK pathway did not seem to be involved in the early phase of hormone treatment. 6) The nonpermeant analog T3-agarose inhibited Na+-K+-ATPase activity in the same way as T3, confirming that hormone signaling initiated at a receptor on the plasma membrane. From these results, it can be concluded that the cell response mechanisms change rapidly and drastically within the early phase of embryo growth. The differences found at the two stages probably reflect the different roles of thyroid hormones during development and differentiation.

Стилі APA, Harvard, Vancouver, ISO та ін.

35

LOMBARDI, Assonta, Antonia LANNI, Maria MORENO, D. Martin BRAND, and Fernando GOGLIA. "Effect of 3,5-di-iodo-L-thyronine on the mitochondrial energy-transduction apparatus." Biochemical Journal 330, no. 1 (February 15, 1998): 521–26. http://dx.doi.org/10.1042/bj3300521.

Повний текст джерела

Анотація:

We examined the effect of a single injection of 3,5-di-iodo-l-thyronine (3,5-T2) (150 μg/100 g body weight) on the rat liver mitochondrial energy-transduction apparatus. We applied ‘top-down’ elasticity analysis, which allows identification of the site of action of an effector within a metabolic pathway. This kinetic approach considers oxidative phosphorylation as two blocks of reactions: those generating the mitochondrial inner-membrane potential (Δψ; ‘substrate oxidation’) and those ‘consuming’ it (‘proton leak’ and ‘phosphorylating system’). The results show that 1 h after the injection of 3,5-T2, state 4 (respiratory state in which there is no ATP synthesis and the exogenous ADP added has been exhausted) and state 3 (respiratory state in which ATP synthesis is at maximal rate) of mitochondrial respiration were significantly increased (by approx. 30%). ‘Top-down’ elasticity analysis revealed that these increases were due to the stimulation of reactions involved in substrate oxidation; neither ‘proton leak’ nor the ‘phosphorylating system’ was influenced by 3,5-T2. Using the same approach we divided the respiratory chain into two blocks of reactions: cytochrome c reducers and cytochrome c oxidizers. We found that both cytochrome c reducers and cytochrome c oxidizers are targets for 3,5-T2. The rapidity with which 3,5-T2 acts in stimulating the mitochondrial respiration rate suggests to us that di-iodo-L-thyronine may play an important role in the physiological conditions in which rapid energy utilization is required, such as cold exposure or overfeeding.

Стилі APA, Harvard, Vancouver, ISO та ін.

36

Silvestri, Elena, Maria Coppola, Angela Ziello, Pasquale Lasala, Cristina Leanza, and Maria Moreno. "Insight on the Body Fat Lowering Effect of 3,5-Diiodo-L-Thyronine." Immunology‚ Endocrine & Metabolic Agents in Medicinal Chemistry 13, no. 3 (December 31, 2013): 159–64. http://dx.doi.org/10.2174/18715222113130990006.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

37

YOUNG, RUTH A., RAJATA RAJATANAVIN, ANDREW F. MORING, and LEWIS E. BRAVERMAN. "Fasting Induces the Generation of Serum Thyronine-Binding Globulin in Zucker Rats*." Endocrinology 116, no. 4 (April 1985): 1248–52. http://dx.doi.org/10.1210/endo-116-4-1248.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

38

ASHITAKA, YOSHIHIKO, MOTOYOSHI MARUO, YASUHITO TAKEUCHI, HIROSHI NAKAYAMA, and MATSUTO MOCHIZUKI. "3,5,3'-Triiodo-L-Thyronine Binding Sites in Nuclei of Human Trophoblastic Cells." Endocrinologia Japonica 35, no. 2 (1988): 197–206. http://dx.doi.org/10.1507/endocrj1954.35.197.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

39

NISHII, HIROSHI, YOSHIHIKO ASHITAKA, MOTOYOSHI MARUO, and MATSUTO MOCHIZUKI. "Studies on the Nuclear 3,5,3'-Triiodo-L-Thyronine Binding Sites in Cytotrophoblast." Endocrinologia Japonica 36, no. 6 (1989): 891–98. http://dx.doi.org/10.1507/endocrj1954.36.891.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

40

Horst, C., H. Rokos, and H. J. Seitz. "Rapid stimulation of hepatic oxygen consumption by 3,5-di-iodo-l-thyronine." Biochemical Journal 261, no. 3 (August 1, 1989): 945–50. http://dx.doi.org/10.1042/bj2610945.

Повний текст джерела

Анотація:

Tri-iodothyronine (T3) and thyroxine (T4) as well as 3,5-di-iodothyronine (T2) stimulated O2 consumption by isolated perfused livers from hypothyroid rats at a concentration as low as 1 pM by about 30% within 90 min. Application of T2 resulted in a faster stimulation than with application of T3 or T4. Inhibition of iodothyronine monodeiodinase by propylthiouracil, thereby blocking the degradation of T4 to T3 and of T3 to T2, demonstrated that only T2 is the active hormone for the rapid stimulation of hepatic O2 consumption: T3 and T4 lost all of their stimulative activity, whereas T2 was as potent as in the absence of propylthiouracil. Perfusion experiments with thyroid-hormone analogues confirmed the specificity of the T2 effect. The nucleus is unlikely to contribute to the rapid T2 effect, as can be deduced from perfusion experiments with cycloheximide and lack of induction of malic enzyme by T2. In conclusion, a new scheme of regulation of mitochondrial activity is proposed: T2 acts rapidly and directly via a mitochondrial pathway, whereas T3 exerts its long-term action indirectly by induction of specific enzymes.

Стилі APA, Harvard, Vancouver, ISO та ін.

41

Lombardi, Assunta, Rosalba Senese, Rita De Matteis, Rosa Anna Busiello, Federica Cioffi, Fernando Goglia, and Antonia Lanni. "3,5-Diiodo-L-Thyronine Activates Brown Adipose Tissue Thermogenesis in Hypothyroid Rats." PLOS ONE 10, no. 2 (February 6, 2015): e0116498. http://dx.doi.org/10.1371/journal.pone.0116498.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

42

Shang, Guoguo, Pan Gao, Zhonghua Zhao, Qi Chen, Tao Jiang, Nong Zhang, and Hui Li. "3,5-Diiodo-l-thyronine ameliorates diabetic nephropathy in streptozotocin-induced diabetic rats." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1832, no. 5 (May 2013): 674–84. http://dx.doi.org/10.1016/j.bbadis.2013.01.023.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

43

Salamonczyk, Grzegorz M., Vibha B. Oza, and Charles J. Sih. "A concise synthesis of thyroxine (T4) and 3,5,3′-Triiodo-l-thyronine (T3)." Tetrahedron Letters 38, no. 40 (October 1997): 6965–68. http://dx.doi.org/10.1016/s0040-4039(97)01665-1.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

44

Chatonnet, Fabrice, Frédéric Picou, Teddy Fauquier, and Frédéric Flamant. "Thyroid Hormone Action in Cerebellum and Cerebral Cortex Development." Journal of Thyroid Research 2011 (2011): 1–8. http://dx.doi.org/10.4061/2011/145762.

Повний текст джерела

Анотація:

Thyroid hormones (TH, including the prohormone thyroxine (T4) and its active deiodinated derivative 3,,5-triiodo-L-thyronine (T3)) are important regulators of vertebrates neurodevelopment. Specific transporters and deiodinases are required to ensure T3 access to the developing brain. T3 activates a number of differentiation processes in neuronal and glial cell types by binding to nuclear receptors, acting directly on transcription. Only few T3 target genes are currently known. Deeper investigations are urgently needed, considering that some chemicals present in food are believed to interfere with T3 signaling with putative neurotoxic consequences.

Стилі APA, Harvard, Vancouver, ISO та ін.

45

Obaid, A., S. Basahl, A. Diefallah, and R. Abu-Eittah. "Spectral Investigations of the Effects of 60Co-Gamma Irradiation on Iodothyronine and Iodotyrosines." Applied Spectroscopy 41, no. 1 (January 1987): 74–79. http://dx.doi.org/10.1366/0003702874867918.

Повний текст джерела

Анотація:

Solids of 3-iodo-, 3–5–di-iodotyrosine and 3,5-di-iodothyronine were irradiated by 60Co-gamma irradiation for a period of about twenty hours. The effects of irradiation were investigated through a study of the UV and IR spectra of irradiated samples. UV spectra showed the presence of a new band at 360 nm which was assigned to the formation of IO−. IR spectra showed a strong carbonyl absorption and the removal of the carboxylate band in the case of thyronine only. For comparison, the spectra of the studied compounds were investigated before irradiation.

Стилі APA, Harvard, Vancouver, ISO та ін.

46

Fanjul, A. N., and R. N. Farías. "Molecular interconversion of cold-sensitive cytosolic 3,3′,5-tri-iodo-l-thyronine-binding proteins from human erythrocytes: effect of cold, heat and pH treatments." Biochemical Journal 290, no. 2 (March 1, 1993): 579–82. http://dx.doi.org/10.1042/bj2900579.

Повний текст джерела

Анотація:

Cytosolic 3,3′,5-tri-iodo-L-thyronine-binding proteins (CTBP I, II and IV species) from human red blood cells undergo rapid loss of activity at low temperatures. Cold treatment of CTBPs was accompanied by dissociation of the polymeric protein to the 60 kDa inactive monomer. Re-activation of the cold-inactivated CTBP IV by warming resulted in association of the monomer to the active polymeric form. A similar association-dissociation phenomenon was also obtained isothermically, though pH changes. We conclude that CTBP I and CTBP II are polymeric forms of CTBP IV.

Стилі APA, Harvard, Vancouver, ISO та ін.

47

Bangur, C. S., J. L. Howland, and S. S. Katyare. "Thyroid hormone treatment alters phospholipid composition and membrane fluidity of rat brain mitochondria." Biochemical Journal 305, no. 1 (January 1, 1995): 29–32. http://dx.doi.org/10.1042/bj3050029.

Повний текст джерела

Анотація:

We examined effects of graded doses of thyroid hormones 3,3′, 5-tri-iodo-L-thyronine (T3) and L-thyroxine (T4) on the lipid composition of rat brain mitochondria. Neither hormone significantly affected the mitochondrial cholesterol or total phospholipid content, but did increase phosphatidylethanolamine (PE) at the expense of phosphatidylserine (PS), phosphatidylinositol (PI) and phosphatidylcholine (PC). The phosphatidic acid (PA) content was also elevated, suggesting enhanced phospholipid turnover. Changes in sphingomyelin (SPM) and diphosphatidylglycerol (DPG) were minimal. Mitochondrial membrane fluidity also increased after thyroid-hormone treatment, and the increase was closely correlated with PC/PE and SPM/PE molar ratios.

Стилі APA, Harvard, Vancouver, ISO та ін.

48

Goglia, F., A. Lanni, C. Horst, M. Moreno, and R. Thoma. "In vitro binding of 3,5-di-iodo-L-thyronine to rat liver mitochondria." Journal of Molecular Endocrinology 13, no. 3 (December 1, 1994): 275–82. http://dx.doi.org/10.1677/jme.0.0130275.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

49

Takeda, T., K. Ichikawa, M. Kobayashi, T. Miyamoto, S. Suzuki, Y. Nishii, A. Sakurai, et al. "Response of hepatic proteins to 3,5,3′-tri-iodo-l-thyronine in diabetic rats." Journal of Endocrinology 143, no. 1 (October 1994): 55–63. http://dx.doi.org/10.1677/joe.0.1430055.

Повний текст джерела

Анотація:

Abstract In order to study whether peripheral action of thyroid hormones is altered in insulin deficiency and to elucidate the biological consequences of alteration of the cytosolic 3,5,3′-tri-iodo-l-thyronine (T3) binding protein (CTBP), we measured malic enzyme, T3-responsive nuclear n protein, CTBP and nuclear thyroid hormone receptor in the liver and kidney of streptozotocin (STZ)-induced diabetic rats that were treated with or without insulin and/or a receptor-saturating dose of T3. The following results were obtained. 1. Induction of malic enzyme by T3 was apparently diminished in diabetic rats. However, supplementary injection of insulin enabled previously given T3 to take effect in diabetic rats. 2. T3-responsiveness of other hepatic proteins (n protein and CTBP) was not altered by insulin in diabetic rats. 3. The level of n protein was increased by insulin in diabetic rats in vivo and in perfused rat liver, indicating that the hepatic n protein is a novel insulin-responsive protein. T3 and insulin increased the level of n protein non-synergistically in diabetic rat liver. 4. Hepatic nuclear receptor levels were not altered in diabetic rats. 5. Hepatic CTBP levels were decreased in diabetic rats. This was not due to the toxic effect of STZ. Low CTBP level was only partially increased by insulin after 30 days of diabetic period. Renal CTBP levels were not altered in diabetic rats with or without insulin treatment. These results indicate that reduction of CTBP did not influence the hepatic response to a receptor-saturating dose of T3, although CTBP may regulate the nuclear T3 transport, and that fundamental action of a receptor-saturating dose of T3 was not attenuated in diabetic rat liver. Journal of Endocrinology (1994) 143, 55–63

Стилі APA, Harvard, Vancouver, ISO та ін.

50

MARCHAND, JEAN, ANNIE GORCE, GABRIEL BADOUAILLE, JEAN-MARC BRAS, DOMINIQUE SIMON, and BERNARD PAU. "Production and Partial Characterization of Monoclonal Antibodies Against 3,3′,5-Triiodo-L-Thyronine." Hybridoma 6, no. 1 (February 1987): 97–101. http://dx.doi.org/10.1089/hyb.1987.6.97.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Ми пропонуємо знижки на всі преміум-плани для авторів, чиї праці увійшли до тематичних добірок літератури. Зв'яжіться з нами, щоб отримати унікальний промокод!