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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] Address:Departamento de Fisiologia e Biofísica, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil.
[Ti] Title: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] Country of publication:England
[La] Language:eng
[Ab] Abstract: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] MeSH terms primary: Blood Glucose/drug effects
Diiodothyronines/pharmacology
Insulin Resistance
[Mh] MeSH terms secundary: Animals
Diet, High-Fat
Energy Metabolism/drug effects
Hep G2 Cells
Humans
Male
Mice
Mice, Inbred C57BL
Obesity
Triiodothyronine/pharmacology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Blood Glucose); 0 (Diiodothyronines); 06LU7C9H1V (Triiodothyronine); 534-51-0 (3,5-diiodothyronine); 70-40-6 (3,3'-diiodothyronine)
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[Js] Journal subset:IM
[Da] Date of entry for processing:161023
[St] Status:MEDLINE
[do] DOI:10.1111/apha.12821

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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] Address:Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
[Ti] Title: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] Country of publication:Italy
[La] Language:eng
[Ab] Abstract: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] MeSH terms primary: Diiodothyronines/pharmacology
Glucose/pharmacology
Insulin-Secreting Cells/secretion
Insulin/secretion
Triiodothyronine/pharmacology
[Mh] MeSH terms secundary: Animals
Cell Line, Tumor
Dose-Response Relationship, Drug
Humans
Rats
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Diiodothyronines); 0 (Insulin); 06LU7C9H1V (Triiodothyronine); 534-51-0 (3,5-diiodothyronine); IY9XDZ35W2 (Glucose)
[Em] Entry month:1708
[Cu] Class update date: 170814
[Lr] Last revision date:170814
[Js] Journal subset:IM
[Da] Date of entry for processing:170708
[St] Status:MEDLINE

  3 / 378 MEDLINE  
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[PMID]: 28362337
[Au] Autor:Damiano F; Rochira A; Gnoni A; Siculella L
[Ad] Address: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] Title: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] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract: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] MeSH terms primary: Diiodothyronines/metabolism
Fatty Acids/metabolism
Liver/metabolism
Thyroxine/metabolism
Triiodothyronine/metabolism
[Mh] MeSH terms secundary: Animals
Humans
Lipid Metabolism
Mitochondria/metabolism
Models, Biological
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Diiodothyronines); 0 (Fatty Acids); 06LU7C9H1V (Triiodothyronine); 534-51-0 (3,5-diiodothyronine); Q51BO43MG4 (Thyroxine)
[Em] Entry month:1706
[Cu] Class update date: 170601
[Lr] Last revision date:170601
[Js] Journal subset:IM
[Da] Date of entry for processing:170401
[St] Status:MEDLINE

  4 / 378 MEDLINE  
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[PMID]: 27854029
[Au] Autor:Cavallo A; Taurino F; Damiano F; Siculella L; Sardanelli AM; Gnoni A
[Ad] Address:Laboratory of Biochemistry and Molecular Biology, Department of Biological and Environmental Sciences and Technologies, University of Salento, Lecce, 73100, Italy.
[Ti] Title: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] Country of publication:United States
[La] Language:eng
[Ab] Abstract: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] MeSH terms primary: Diiodothyronines/pharmacology
Energy Metabolism/drug effects
Hypothyroidism/drug therapy
Mitochondria, Liver/metabolism
[Mh] MeSH terms secundary: Animals
Diiodothyronines/administration & dosage
Electron Transport/drug effects
Fatty Acids/metabolism
Oxidation-Reduction/drug effects
Oxidative Stress/drug effects
Rats
Uncoupling Agents/pharmacology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Diiodothyronines); 0 (Fatty Acids); 0 (Uncoupling Agents); 534-51-0 (3,5-diiodothyronine)
[Em] Entry month:1704
[Cu] Class update date: 171021
[Lr] Last revision date:171021
[Js] Journal subset:IM
[Da] Date of entry for processing:161118
[St] Status:MEDLINE

  5 / 378 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] Address:Institute for Community Medicine, University Medicine Greifswald, Walther Rathenau Str. 48, D-17475, Greifswald, Germany. till.ittermann@uni-greifswald.de.
[Ti] Title: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] Country of publication:Germany
[La] Language:eng
[Ab] Abstract: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] MeSH terms primary: Aorta/diagnostic imaging
Aortic Diseases/diagnostic imaging
Atherosclerosis/diagnostic imaging
Thyrotropin/blood
[Mh] MeSH terms secundary: Adult
Aged
Aged, 80 and over
Aorta/pathology
Aortic Diseases/pathology
Atherosclerosis/pathology
Diiodothyronines/blood
Female
Humans
Magnetic Resonance Imaging
Male
Middle Aged
Multivariate Analysis
Organ Size
Young Adult
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Diiodothyronines); 534-51-0 (3,5-diiodothyronine); 9002-71-5 (Thyrotropin)
[Em] Entry month:1702
[Cu] Class update date: 171010
[Lr] Last revision date:171010
[Js] Journal subset:IM
[Da] Date of entry for processing:160315
[St] Status:MEDLINE

  6 / 378 MEDLINE  
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[PMID]: 26903510
[Au] Autor:Lietzow J; Golchert J; Homuth G; Völker U; Jonas W; Köhrle J
[Ad] Address:Institut für Experimentelle EndokrinologieCharité - Universitätsmedizin Berlin, Berlin, Germany.
[Ti] Title: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] Country of publication:England
[La] Language:eng
[Ab] Abstract: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] MeSH terms primary: Diiodothyronines/pharmacology
Energy Metabolism/drug effects
Energy Metabolism/genetics
Gene Expression Regulation/drug effects
Steroids/metabolism
Thyroid Hormones/metabolism
Xenobiotics/metabolism
[Mh] MeSH terms secundary: Animals
Bile Acids and Salts/biosynthesis
Cytochrome P-450 Enzyme System/genetics
Cytochrome P-450 Enzyme System/metabolism
Gene Expression Profiling
Gene Expression Regulation, Enzymologic/drug effects
Hepatocytes/metabolism
Liver/metabolism
Male
Mice
Obesity/genetics
Obesity/metabolism
Pharmacogenetics
Transcriptome
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance: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] Entry month:1710
[Cu] Class update date: 171026
[Lr] Last revision date:171026
[Js] Journal subset:IM
[Da] Date of entry for processing:160224
[St] Status:MEDLINE
[do] DOI:10.1530/JME-15-0159

  7 / 378 MEDLINE  
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[PMID]: 26820127
[Au] Autor:Hernández-Puga G; Navarrete-Ramírez P; Mendoza A; Olvera A; Villalobos P; Orozco A
[Ad] Address:Instituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM), Boulevard Juriquilla 3001, Querétaro, Qro. 76230, Mexico.
[Ti] Title: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] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract: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] MeSH terms primary: Diiodothyronines/pharmacology
Hydrocortisone/pharmacology
Thyroid Hormone Receptors beta/genetics
Tilapia/metabolism
[Mh] MeSH terms secundary: Animals
Computer Simulation
Fish Proteins/metabolism
Gene Expression Regulation/drug effects
Promoter Regions, Genetic
Response Elements
Signal Transduction/drug effects
Thyroid Hormone Receptors beta/metabolism
Tilapia/genetics
Transcription, Genetic/drug effects
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Diiodothyronines); 0 (Fish Proteins); 0 (Thyroid Hormone Receptors beta); 534-51-0 (3,5-diiodothyronine); WI4X0X7BPJ (Hydrocortisone)
[Em] Entry month:1612
[Cu] Class update date: 161230
[Lr] Last revision date:161230
[Js] Journal subset:IM
[Da] Date of entry for processing:160129
[St] Status:MEDLINE

  8 / 378 MEDLINE  
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[PMID]: 26593437
[Au] Autor:Coppola M; Cioffi F; Moreno M; Goglia F; Silvestri E
[Ti] Title:3,5-diiodo-L-thyronine: A Possible Pharmacological Agent?
[So] Source:Curr Drug Deliv;13(3):330-8, 2016.
[Is] ISSN:1875-5704
[Cp] Country of publication:United Arab Emirates
[La] Language:eng
[Ab] Abstract: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] MeSH terms primary: Anti-Obesity Agents/pharmacology
Diiodothyronines/pharmacology
Hypolipidemic Agents/pharmacology
[Mh] MeSH terms secundary: Animals
Diiodothyronines/metabolism
Humans
Hypothalamo-Hypophyseal System/metabolism
Thyroid Gland/metabolism
Triiodothyronine/metabolism
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Anti-Obesity Agents); 0 (Diiodothyronines); 0 (Hypolipidemic Agents); 06LU7C9H1V (Triiodothyronine); 534-51-0 (3,5-diiodothyronine)
[Em] Entry month:1702
[Cu] Class update date: 170215
[Lr] Last revision date:170215
[Js] Journal subset:IM
[Da] Date of entry for processing:151124
[St] Status:MEDLINE

  9 / 378 MEDLINE  
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[PMID]: 26485433
[Au] Autor:Vatner DF; Snikeris J; Popov V; Perry RJ; Rahimi Y; Samuel VT
[Ad] Address:Department of Internal Medicine,Yale University School of Medicine, New Haven, CT, United States of America.
[Ti] Title: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] Country of publication:United States
[La] Language:eng
[Ab] Abstract: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] MeSH terms primary: Body Composition/drug effects
Diiodothyronines/pharmacology
Fatty Liver/prevention & control
Insulin Resistance
Liver/drug effects
[Mh] MeSH terms secundary: Animals
Body Weight/drug effects
Diet, High-Fat
Diiodothyronines/therapeutic use
Insulin/blood
Lipid Metabolism/drug effects
Liver/metabolism
Male
Rats
Rats, Sprague-Dawley
Triglycerides/blood
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Name of substance:0 (Diiodothyronines); 0 (Insulin); 0 (Triglycerides); 534-51-0 (3,5-diiodothyronine)
[Em] Entry month:1606
[Cu] Class update date: 161019
[Lr] Last revision date:161019
[Js] Journal subset:IM
[Da] Date of entry for processing:151021
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0140837

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[PMID]: 26347660
[Au] Autor:Lombardi A; Moreno M; de Lange P; Iossa S; Busiello RA; Goglia F
[Ad] Address:Department of Biology, University of Naples Federico II Naples, Italy.
[Ti] Title:Regulation of skeletal muscle mitochondrial activity by thyroid hormones: focus on the "old" triiodothyronine and the "emerging" 3,5-diiodothyronine.
[So] Source:Front Physiol;6:237, 2015.
[Is] ISSN:1664-042X
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:3,5,3'-Triiodo-L-thyronine (T3) plays a crucial role in regulating metabolic rate and fuel oxidation; however, the mechanisms by which it affects whole-body energy metabolism are still not completely understood. Skeletal muscle (SKM) plays a relevant role in energy metabolism and responds to thyroid state by remodeling the metabolic characteristics and cytoarchitecture of myocytes. These processes are coordinated with changes in mitochondrial content, bioenergetics, substrate oxidation rate, and oxidative phosphorylation efficiency. Recent data indicate that "emerging" iodothyronines have biological activity. Among these, 3,5-diiodo-L-thyronine (T2) affects energy metabolism, SKM substrate utilization, and mitochondrial functionality. The effects it exerts on SKM mitochondria involve more aspects of mitochondrial bioenergetics; among these, respiratory chain activity, mitochondrial thermogenesis, and lipid-handling are stimulated rapidly. This mini review focuses on signaling and biochemical pathways activated by T3 and T2 in SKM that influence the above processes. These novel aspects of thyroid physiology could reveal new perspectives for understanding the involvement of SKM mitochondria in hypo- and hyper-thyroidism.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1509
[Cu] Class update date: 170220
[Lr] Last revision date:170220
[Da] Date of entry for processing:150909
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.3389/fphys.2015.00237


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