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Pesquisa : D06.472.931.740.180 [Categoria DeCS]
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  1 / 371 MEDLINE  
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[PMID]:27770485
[Au] Autor:da Silva Teixeira S; Filgueira C; Sieglaff DH; Benod C; Villagomez R; Minze LJ; Zhang A; Webb P; Nunes MT
[Ad] Endereço:Departamento de Fisiologia e Biofísica, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil.
[Ti] Título:3,5-diiodothyronine (3,5-T2) reduces blood glucose independently of insulin sensitization in obese mice.
[So] Source:Acta Physiol (Oxf);220(2):238-250, 2017 Jun.
[Is] ISSN:1748-1716
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIM: Thyroid hormones regulate metabolic response. While triiodothyronine (T3) is usually considered to be the active form of thyroid hormone, one form of diiodothyronine (3,5-T2) exerts T3-like effects on energy consumption and lipid metabolism. 3,5-T2 also improves glucose tolerance in rats and 3,5-T2 levels correlate with fasting glucose in humans. Presently, however, little is known about mechanisms of 3,5-T2 effects on glucose metabolism. Here, we set out to compare effects of T3, 3,5-T2 and another form of T2 (3,3-T2) in a mouse model of diet-induced obesity and determined effects of T3 and 3,5-T2 on markers of classical insulin sensitization to understand how diiodothyronines influence blood glucose. METHODS: Cell- and protein-based assays of thyroid hormone action. Assays of metabolic parameters in mice. Analysis of transcript and protein levels in different tissues by qRT-PCR and Western blot. RESULTS: T3 and 3,5-T2 both reduce body weight, adiposity and body temperature despite increased food intake. 3,3'-T2 lacks these effects. T3 and 3,5-T2 reduce blood glucose levels, whereas 3,3'-T2 worsens glucose tolerance. Neither T3 nor 3,5-T2 affects markers of insulin sensitization in skeletal muscle or white adipose tissue (WAT), but both reduce hepatic GLUT2 glucose transporter levels and glucose output. T3 and 3,5-T2 also induce expression of mitochondrial uncoupling proteins (UCPs) 3 and 1 in skeletal muscle and WAT respectively. CONCLUSIONS: 3,5-T2 influences glucose metabolism in a manner that is distinct from insulin sensitization and involves reductions in hepatic glucose output and changes in energy utilization.
[Mh] Termos MeSH primário: Glicemia/efeitos dos fármacos
Di-Iodotironinas/farmacologia
Resistência à Insulina
[Mh] Termos MeSH secundário: Animais
Dieta Hiperlipídica
Metabolismo Energético/efeitos dos fármacos
Células Hep G2
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Obesidade
Tri-Iodotironina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Diiodothyronines); 06LU7C9H1V (Triiodothyronine); 534-51-0 (3,5-diiodothyronine); 70-40-6 (3,3'-diiodothyronine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1111/apha.12821


  2 / 371 MEDLINE  
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[PMID]:28685559
[Au] Autor:Fallahi P; Ferrari SM; Santini E; Camastra S; Frenzilli G; Puccini M; Goglia F; Lanni A; Marchetti P; Antonelli A
[Ad] Endereço:Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
[Ti] Título:Both 3,5-diiodo-L-thyronine (T2) and T3 modulate glucose-induced insulin secretion.
[So] Source:J Biol Regul Homeost Agents;31(2):503-508, 2017 Apr-Jun.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:3,5-diiodo-L-thyronine (T2), a naturally existing iodothyronine, has biological effects on humans, but no information is available on its action on pancreatic b-cells. We evaluated its effect vs triiodothyronine (T3), on glucose-induced insulin secretion in INS-1e cells, a rat insulinoma line, and on human islets. INS-1e were incubated in the presence/absence of T2 or T3 (0.1 nmol/L-10 µmol/L), and glucose (3.3, 7.5, 11.0, and 20 mmol/L). Insulin release and content (at 11.0 and 20 mmol/L glucose) were significantly (p less than 0.01) stimulated by 1-100 nmol/L T2 and 0.1 nmol/L-1.0 µmol/L T3, and inhibited with higher concentrations of both (1–10 µmol/L T2 and 10 µmol/L T3). Human islets were incubated with 3.3 mmol/L glucose in presence/absence of T3 or T2 (0.1 nmol/L, 0.1 µmol/L, and 1 µmol/L). T2 (0.1 nmol/L-0.1 µmol/L) significantly (p less than0.01) stimulated insulin secretion, while higher concentrations (1 µmol/L) inhibited it. A modest increase in insulin secretion was evidenced with 1 µmol/L T3. In conclusion, T2 and T3 have a direct regulatory role in insulin secretion, depending on their concentrations and the glucose level itself. At concentrations near the physiological range, T2 enhances glucose-induced insulin secretion in both rat b-cells and human islets.
[Mh] Termos MeSH primário: Di-Iodotironinas/farmacologia
Glucose/farmacologia
Células Secretoras de Insulina/secreção
Insulina/secreção
Tri-Iodotironina/farmacologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Relação Dose-Resposta a Droga
Seres Humanos
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Diiodothyronines); 0 (Insulin); 06LU7C9H1V (Triiodothyronine); 534-51-0 (3,5-diiodothyronine); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE


  3 / 371 MEDLINE  
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[PMID]:28362337
[Au] Autor:Damiano F; Rochira A; Gnoni A; Siculella L
[Ad] Endereço:Laboratory of Biochemistry and Molecular Biology, Department of Biological and Environmental Sciences and Technologies, University of Salento, 73100 Lecce, Italy. fabrizio.damiano@unisalento.it.
[Ti] Título:Action of Thyroid Hormones, T3 and T2, on Hepatic Fatty Acids: Differences in Metabolic Effects and Molecular Mechanisms.
[So] Source:Int J Mol Sci;18(4), 2017 Mar 31.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The thyroid hormones (THs) 3,3',5,5'-tetraiodo-l-thyronine (T4) and 3,5,3'-triiodo-l-thyronine (T3) influence many metabolic pathways. The major physiological function of THs is to sustain basal energy expenditure, by acting primarily on carbohydrate and lipid catabolism. Beyond the mobilization and degradation of lipids, at the hepatic level THs stimulate the de novo fatty acid synthesis (de novo lipogenesis, DNL), through both the modulation of gene expression and the rapid activation of cell signalling pathways. 3,5-Diiodo-l-thyronine (T2), previously considered only a T3 catabolite, has been shown to mimic some of T3 effects on lipid catabolism. However, T2 action is more rapid than that of T3, and seems to be independent of protein synthesis. An inhibitory effect on DNL has been documented for T2. Here, we give an overview of the mechanisms of THs action on liver fatty acid metabolism, focusing on the different effects exerted by T2 and T3 on the regulation of the DNL. The inhibitory action on DNL exerted by T2 makes this compound a potential and attractive drug for the treatment of some metabolic diseases and cancer.
[Mh] Termos MeSH primário: Di-Iodotironinas/metabolismo
Ácidos Graxos/metabolismo
Fígado/metabolismo
Tiroxina/metabolismo
Tri-Iodotironina/metabolismo
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Metabolismo dos Lipídeos
Mitocôndrias/metabolismo
Modelos Biológicos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Diiodothyronines); 0 (Fatty Acids); 06LU7C9H1V (Triiodothyronine); 534-51-0 (3,5-diiodothyronine); Q51BO43MG4 (Thyroxine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170601
[Lr] Data última revisão:
170601
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170401
[St] Status:MEDLINE


  4 / 371 MEDLINE  
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[PMID]:27854029
[Au] Autor:Cavallo A; Taurino F; Damiano F; Siculella L; Sardanelli AM; Gnoni A
[Ad] Endereço:Laboratory of Biochemistry and Molecular Biology, Department of Biological and Environmental Sciences and Technologies, University of Salento, Lecce, 73100, Italy.
[Ti] Título:Acute administration of 3,5-diiodo-L-thyronine to hypothyroid rats stimulates bioenergetic parameters in liver mitochondria.
[So] Source:J Bioenerg Biomembr;48(5):521-529, 2016 10.
[Is] ISSN:1573-6881
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The role of 3,5-diiodo-L-thyronine (T ), initially considered only a 3,3',5-triiodo-L-thyronine (T ) catabolite, in the bioenergetic metabolism is of growing interest. In this study we investigated the acute effects (within 1 h) of T administration to hypothyroid rats on liver mitochondria fatty acid uptake and ß-oxidation rate, mitochondrial efficiency (by measuring proton leak) and mitochondrial oxidative damage (by determining H O release). Fatty acid uptake into mitochondria was measured assaying carnitine palmitoyl transferase (CPT) I and II activities, and fatty acid ß-oxidation using palmitoyl-CoA as a respiratory substrate. Mitochondrial fatty acid pattern was defined by gas-liquid chromatography. In hypothyroid + T vs hypothyroid rats we observed a raise in the serum level of nonesterified fatty acids (NEFA), in the mitochondrial CPT system activity and in the fatty acid ß-oxidation rate. A parallel increase in the respiratory chain activity, mainly from succinate, occurs. When fatty acids are chelated by bovine serum albumin, a T -induced increase in both state 3 and state 4 respiration is observed, while, when fatty acids are present, mitochondrial uncoupling occurs together with increased proton leak, responsible for mitochondrial thermogenesis. T administration decreases mitochondrial oxidative stress as determined by lower H O production. We conclude that in rat liver mitochondria T acutely enhances the rate of fatty acid ß-oxidation, and the activity of the downstream respiratory chain. The T -induced increase in proton leak may contribute to mitochondrial thermogenesis and to the reduction of oxidative stress. Our results strengthen the previously reported ability of T to reduce adiposity, dyslipidemia and to prevent liver steatosis.
[Mh] Termos MeSH primário: Di-Iodotironinas/farmacologia
Metabolismo Energético/efeitos dos fármacos
Hipotireoidismo/tratamento farmacológico
Mitocôndrias Hepáticas/metabolismo
[Mh] Termos MeSH secundário: Animais
Di-Iodotironinas/administração & dosagem
Transporte de Elétrons/efeitos dos fármacos
Ácidos Graxos/metabolismo
Oxirredução/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
Ratos
Desacopladores/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Diiodothyronines); 0 (Fatty Acids); 0 (Uncoupling Agents); 534-51-0 (3,5-diiodothyronine)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171021
[Lr] Data última revisão:
171021
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161118
[St] Status:MEDLINE


  5 / 371 MEDLINE  
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[PMID]:26973144
[Au] Autor:Ittermann T; Lorbeer R; Dörr M; Schneider T; Quadrat A; Heßelbarth L; Wenzel M; Lehmphul I; Köhrle J; Mensel B; Völzke H
[Ad] Endereço:Institute for Community Medicine, University Medicine Greifswald, Walther Rathenau Str. 48, D-17475, Greifswald, Germany. till.ittermann@uni-greifswald.de.
[Ti] Título:High levels of thyroid-stimulating hormone are associated with aortic wall thickness in the general population.
[So] Source:Eur Radiol;26(12):4490-4496, 2016 Dec.
[Is] ISSN:1432-1084
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Our aim was to investigate the association of thyroid function defined by serum concentrations of thyroid-stimulating hormone (TSH) with thoracic aortic wall thickness (AWT) as a marker of atherosclerotic processes. METHODS: We pooled data of 2,679 individuals from two independent population-based surveys of the Study of Health in Pomerania. Aortic diameter and AWT measurements were performed on a 1.5-T MRI scanner at the concentration of the right pulmonary artery displaying the ascending and the descending aorta. RESULTS: TSH, treated as continuous variable, was significantly associated with descending AWT (ß = 0.11; 95 % confidence interval (CI) 0.02-0.21), while the association with ascending AWT was not statistically significant (ß = 0.20; 95 % CI -0.01-0.21). High TSH (>3.29 mIU/L) was significantly associated with ascending (ß = 0.12; 95 % CI 0.02-0.23) but not with descending AWT (ß = 0.06; 95 % CI -0.04-0.16). There was no consistent association between TSH and aortic diameters. CONCLUSIONS: Our study demonstrated that AWT values increase with increasing serum TSH concentrations. Thus, a hypothyroid state may be indicative for aortic atherosclerosis. These results fit very well to the findings of previous studies pointing towards increased atherosclerotic risk in the hypothyroid state. KEY POINTS: • Serum TSH concentrations are positively associated with aortic wall thickness. • Serum TSH concentrations are not associated with the aortic diameters. • Serum 3,5-diiodothyronine concentrations may be positively associated with aortic wall thickness.
[Mh] Termos MeSH primário: Aorta/diagnóstico por imagem
Doenças da Aorta/diagnóstico por imagem
Aterosclerose/diagnóstico por imagem
Tireotropina/sangue
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Aorta/patologia
Doenças da Aorta/patologia
Aterosclerose/patologia
Di-Iodotironinas/sangue
Feminino
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Análise Multivariada
Tamanho do Órgão
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Diiodothyronines); 534-51-0 (3,5-diiodothyronine); 9002-71-5 (Thyrotropin)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160315
[St] Status:MEDLINE


  6 / 371 MEDLINE  
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[PMID]:26903510
[Au] Autor:Lietzow J; Golchert J; Homuth G; Völker U; Jonas W; Köhrle J
[Ad] Endereço:Institut für Experimentelle EndokrinologieCharité - Universitätsmedizin Berlin, Berlin, Germany.
[Ti] Título:3,5-T2 alters murine genes relevant for xenobiotic, steroid, and thyroid hormone metabolism.
[So] Source:J Mol Endocrinol;56(4):311-23, 2016 May.
[Is] ISSN:1479-6813
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The endogenous thyroid hormone (TH) metabolite 3,5-diiodo-l-thyronine (3,5-T2) 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-T2 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-T2 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-T2 Our results revealed that 3,5-T2 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-T2 changes the expression of TH responsive genes, suggesting a thyromimetic action of 3,5-T2 in mouse liver. Interestingly, 3,5-T2 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-T2 in steroid metabolism of obese mice. We concluded that treatment with 3,5-T2 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-T2 might exert adverse hepatic effects. Accordingly, the conceivable use of 3,5-T2 as pharmacological hypolipidemic agent should be considered with caution.
[Mh] Termos MeSH primário: Di-Iodotironinas/farmacologia
Metabolismo Energético/efeitos dos fármacos
Metabolismo Energético/genética
Regulação da Expressão Gênica/efeitos dos fármacos
Esteroides/metabolismo
Hormônios Tireóideos/metabolismo
Xenobióticos/metabolismo
[Mh] Termos MeSH secundário: Animais
Ácidos e Sais Biliares/biossíntese
Sistema Enzimático do Citocromo P-450/genética
Sistema Enzimático do Citocromo P-450/metabolismo
Perfilação da Expressão Gênica
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Hepatócitos/metabolismo
Fígado/metabolismo
Masculino
Camundongos
Obesidade/genética
Obesidade/metabolismo
Farmacogenética
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bile Acids and Salts); 0 (Diiodothyronines); 0 (Steroids); 0 (Thyroid Hormones); 0 (Xenobiotics); 534-51-0 (3,5-diiodothyronine); 9035-51-2 (Cytochrome P-450 Enzyme System)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160224
[St] Status:MEDLINE
[do] DOI:10.1530/JME-15-0159


  7 / 371 MEDLINE  
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[PMID]:26820127
[Au] Autor:Hernández-Puga G; Navarrete-Ramírez P; Mendoza A; Olvera A; Villalobos P; Orozco A
[Ad] Endereço:Instituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM), Boulevard Juriquilla 3001, Querétaro, Qro. 76230, Mexico.
[Ti] Título:3,5-Diiodothyronine-mediated transrepression of the thyroid hormone receptor beta gene in tilapia. Insights on cross-talk between the thyroid hormone and cortisol signaling pathways.
[So] Source:Mol Cell Endocrinol;425:103-10, 2016 Apr 15.
[Is] ISSN:1872-8057
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:T3 and cortisol activate or repress gene expression in virtually every vertebrate cell mainly by interacting with their nuclear hormone receptors. In contrast to the mechanisms for hormone gene activation, the mechanisms involved in gene repression remain elusive. In teleosts, the thyroid hormone receptor beta gene or thrb produces two isoforms of TRß1 that differ by nine amino acids in the ligand-binding domain of the long-TRß1, whereas the short-TRß1 lacks the insert. Previous reports have shown that the genomic effects exerted by 3,5-T2, a product of T3 outer-ring deiodination, are mediated by the long-TRß1. Furthermore, 3,5-T2 and T3 down-regulate the expression of long-TRß1 and short-TRß1, respectively. In contrast, cortisol has been shown to up-regulate the expression of thrb. To understand the molecular mechanisms for thrb modulation by thyroid hormones and cortisol, we used an in silico approach to identify thyroid- and cortisol-response elements within the proximal promoter of thrb from tilapia. We then characterized the identified response elements by EMSA and correlated our observations with the effects of THs and cortisol upon expression of thrb in tilapia. Our data show that 3,5-T2 represses thrb expression and impairs its up-regulation by cortisol possibly through a transrepression mechanism. We propose that for thrb down-regulation, ligands other than T3 are required to orchestrate the pleiotropic effects of thyroid hormones in vertebrates.
[Mh] Termos MeSH primário: Di-Iodotironinas/farmacologia
Hidrocortisona/farmacologia
Receptores beta dos Hormônios Tireóideos/genética
Tilápia/metabolismo
[Mh] Termos MeSH secundário: Animais
Simulação por Computador
Proteínas de Peixes/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Regiões Promotoras Genéticas
Elementos de Resposta
Transdução de Sinais/efeitos dos fármacos
Receptores beta dos Hormônios Tireóideos/metabolismo
Tilápia/genética
Transcrição Genética/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Diiodothyronines); 0 (Fish Proteins); 0 (Thyroid Hormone Receptors beta); 534-51-0 (3,5-diiodothyronine); WI4X0X7BPJ (Hydrocortisone)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160129
[St] Status:MEDLINE


  8 / 371 MEDLINE  
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[PMID]:26593437
[Au] Autor:Coppola M; Cioffi F; Moreno M; Goglia F; Silvestri E
[Ti] Título:3,5-diiodo-L-thyronine: A Possible Pharmacological Agent?
[So] Source:Curr Drug Deliv;13(3):330-8, 2016.
[Is] ISSN:1875-5704
[Cp] País de publicação:United Arab Emirates
[La] Idioma:eng
[Ab] Resumo:Overweight and obesity related metabolic disorders, commonly sharing a pathogenic excess of body adiposity, are world-wide epidemic leading to increasing morbidity and mortality. The related conditions include, among the others, liver steatosis, insulin resistance, and cardiovascular risk. Effective and safe anti-obesity drugs are still needed. Likely without undesirable side effects, an ideal treatment should be able to counteract the numerous causes associated with excess of body adiposity putatively modulating the delicate balance between feeding and energy expenditure, untimely controlling the adipose mass. In the past, thyroid hormones have been tested in reducing weight and lipid accumulation, however, the concomitant induction of a thyrotoxicosis state limited their use. Recent studies in rodents revealed that 3,5- diiodo-L-thyronine (T2), an endogenous metabolite of thyroid hormones, exhibits interesting metabolic activities. Specifically, when exogenously administered, T2 increases the resting metabolic rate and elicits short-term beneficial hypolipidemic effects, without being thyrotoxic, at lest in high fat diet fed rats. Now, a matter of interest is whether T2 can be considered or not a potential anti-obesity pharmacological agent. Actually, very few studies have been performed as far as it concerns the effects of T2 in humans and further analyses on larger cohorts to test time of use- and dose-dependent actions as well as the putative occurrence of T2 induced undesirable side effects, are needed. Here, an updated overview of the current literature on T2 bioactivity is furnished with a particular focus on those effects which may be defined "beneficial" vs. "deleterious" ones above all in view of its putative pharmacological use.
[Mh] Termos MeSH primário: Fármacos Antiobesidade/farmacologia
Di-Iodotironinas/farmacologia
Hipolipemiantes/farmacologia
[Mh] Termos MeSH secundário: Animais
Di-Iodotironinas/metabolismo
Seres Humanos
Sistema Hipotálamo-Hipofisário/metabolismo
Glândula Tireoide/metabolismo
Tri-Iodotironina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Obesity Agents); 0 (Diiodothyronines); 0 (Hypolipidemic Agents); 06LU7C9H1V (Triiodothyronine); 534-51-0 (3,5-diiodothyronine)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170215
[Lr] Data última revisão:
170215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151124
[St] Status:MEDLINE


  9 / 371 MEDLINE  
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[PMID]:26485433
[Au] Autor:Vatner DF; Snikeris J; Popov V; Perry RJ; Rahimi Y; Samuel VT
[Ad] Endereço:Department of Internal Medicine,Yale University School of Medicine, New Haven, CT, United States of America.
[Ti] Título:3,5 Diiodo-L-Thyronine (T2) Does Not Prevent Hepatic Steatosis or Insulin Resistance in Fat-Fed Sprague Dawley Rats.
[So] Source:PLoS One;10(10):e0140837, 2015.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thyroid hormone mimetics are alluring potential therapies for diseases like dyslipidemia, nonalcoholic fatty liver disease (NAFLD), and insulin resistance. Though diiodothyronines are thought inactive, pharmacologic treatment with 3,5- Diiodo-L-Thyronine (T2) reportedly reduces hepatic lipid content and improves glucose tolerance in fat-fed male rats. To test this, male Sprague Dawley rats fed a safflower-oil based high-fat diet were treated with T2 (0.25 mg/kg-d) or vehicle. Neither 10 nor 30 days of T2 treatment had an effect on weight, adiposity, plasma fatty acids, or hepatic steatosis. Insulin action was quantified in vivo by a hyperinsulinemic-euglycemic clamp. T2 did not alter fasting plasma glucose or insulin concentration. Basal endogenous glucose production (EGP) rate was unchanged. During the clamp, there was no difference in insulin stimulated whole body glucose disposal. Insulin suppressed EGP by 60% ± 10 in T2-treated rats as compared with 47% ± 4 suppression in the vehicle group (p = 0.32). This was associated with an improvement in hepatic insulin signaling; insulin stimulated Akt phosphorylation was ~2.5 fold greater in the T2-treated group as compared with the vehicle-treated group (p = 0.003). There was no change in expression of genes thought to mediate the effect of T2 on hepatic metabolism, including genes that regulate hepatic lipid oxidation (ppara, carnitine palmitoyltransferase 1a), genes that regulate hepatic fatty acid synthesis (srebp1c, acetyl coa carboxylase, fatty acid synthase), and genes involved in glycolysis and gluconeogenesis (L-pyruvate kinase, glucose 6 phosphatase). Therefore, in contrast with previous reports, in Sprague Dawley rats fed an unsaturated fat diet, T2 administration failed to improve NAFLD or whole body insulin sensitivity. Though there was a modest improvement in hepatic insulin signaling, this was not associated with significant differences in hepatic insulin action. Further study will be necessary before diiodothyronines can be considered an effective treatment for NAFLD and dyslipidemia.
[Mh] Termos MeSH primário: Composição Corporal/efeitos dos fármacos
Di-Iodotironinas/farmacologia
Fígado Gorduroso/prevenção & controle
Resistência à Insulina
Fígado/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Peso Corporal/efeitos dos fármacos
Dieta Hiperlipídica
Di-Iodotironinas/uso terapêutico
Insulina/sangue
Metabolismo dos Lipídeos/efeitos dos fármacos
Fígado/metabolismo
Masculino
Ratos
Ratos Sprague-Dawley
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Diiodothyronines); 0 (Insulin); 0 (Triglycerides); 534-51-0 (3,5-diiodothyronine)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151021
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0140837


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[PMID]:26322373
[Au] Autor:Ferrara AM; Liao XH; Ye H; Weiss RE; Dumitrescu AM; Refetoff S
[Ad] Endereço:Departments of Medicine (A.M.F., X.-H.L., H.Y., R.E.W., A.M.D., S.R.) and Pediatrics (R.E.W., S.R.) and the Committee on Genetics (S.R.), The University of Chicago, Chicago, Illinois 60637.
[Ti] Título:The Thyroid Hormone Analog DITPA Ameliorates Metabolic Parameters of Male Mice With Mct8 Deficiency.
[So] Source:Endocrinology;156(11):3889-94, 2015 Nov.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mutations in the gene encoding the thyroid hormone (TH) transporter, monocarboxylate transporter 8 (MCT8), cause mental retardation in humans associated with a specific thyroid hormone phenotype manifesting high serum T3 and low T4 and rT3 levels. Moreover, these patients have failure to thrive, and physiological changes compatible with thyrotoxicosis. Recent studies in Mct8-deficient (Mct8KO) mice revealed that the high serum T3 causes increased energy expenditure. The TH analog, diiodothyropropionic acid (DITPA), enters cells independently of Mct8 transport and shows thyromimetic action but with a lower metabolic activity than TH. In this study DITPA was given daily ip to adult Mct8KO mice to determine its effect on thyroid tests in serum and metabolism (total energy expenditure, respiratory exchange rate, and food and water intake). In addition, we measured the expression of TH-responsive genes in the brain, liver, and muscles to assess the thyromimetic effects of DITPA. Administration of 0.3 mg DITPA per 100 g body weight to Mct8KO mice brought serum T3 levels and the metabolic parameters studied to levels observed in untreated Wt animals. Analysis of TH target genes revealed amelioration of the thyrotoxic state in liver, somewhat in the soleus, but there was no amelioration of the brain hypothyroidism. In conclusion, at the dose used, DITPA mainly ameliorated the hypermetabolism of Mct8KO mice. This thyroid hormone analog is suitable for the treatment of the hypermetabolism in patients with MCT8 deficiency, as suggested in limited preliminary human trials.
[Mh] Termos MeSH primário: Di-Iodotironinas/farmacologia
Proteínas de Membrana Transportadoras/deficiência
Retardo Mental Ligado ao Cromossomo X/prevenção & controle
Hipotonia Muscular/prevenção & controle
Atrofia Muscular/prevenção & controle
Propionatos/farmacologia
[Mh] Termos MeSH secundário: Animais
Encéfalo/efeitos dos fármacos
Encéfalo/metabolismo
Di-Iodotironinas/administração & dosagem
Ingestão de Líquidos/efeitos dos fármacos
Ingestão de Alimentos/efeitos dos fármacos
Metabolismo Energético/efeitos dos fármacos
Expressão Gênica/efeitos dos fármacos
Glutationa Transferase/genética
Glicerol-3-Fosfato Desidrogenase (NAD+)/genética
Seres Humanos
Injeções Intraperitoneais
Isoenzimas/genética
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Proteínas de Membrana Transportadoras/genética
Retardo Mental Ligado ao Cromossomo X/sangue
Retardo Mental Ligado ao Cromossomo X/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Knockout
Hipotonia Muscular/sangue
Hipotonia Muscular/metabolismo
Músculo Esquelético/efeitos dos fármacos
Músculo Esquelético/metabolismo
Atrofia Muscular/sangue
Atrofia Muscular/metabolismo
Propionatos/administração & dosagem
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Hormônios Tireóideos/sangue
Tireotropina/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Diiodothyronines); 0 (Isoenzymes); 0 (Membrane Transport Proteins); 0 (Propionates); 0 (Slc16a2 protein, mouse); 0 (Thyroid Hormones); 1HTO2X0SJ9 (3,5-diiodothyropropionic acid); 9002-71-5 (Thyrotropin); EC 1.1.1.8 (Glycerol-3-Phosphate Dehydrogenase (NAD+)); EC 2.5.1.18 (Glutathione Transferase); EC 2.5.1.18 (glutathione S-transferase alpha)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:150901
[St] Status:MEDLINE
[do] DOI:10.1210/en.2015-1234



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