Bibliografías temáticas / Thiazolidinedione (TZD)

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Literatura académica sobre el tema "Thiazolidinedione (TZD)"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 16 de febrero de 2022

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Artículos de revistas sobre el tema "Thiazolidinedione (TZD)"

Rahman, Safikur, Md Tabish Rehman, Gulam Rabbani, Parvez Khan, Mohamed F. AlAjmi, Md Imtaiyaz Hassan, Ghazala Muteeb y Jihoe Kim. "Insight of the Interaction between 2,4-thiazolidinedione and Human Serum Albumin: A Spectroscopic, Thermodynamic and Molecular Docking Study". International Journal of Molecular Sciences 20, n.º 11 (3 de junio de 2019): 2727. http://dx.doi.org/10.3390/ijms20112727.

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Thiazolidinedione derivatives (TZDs) have attracted attention because of their pharmacological effects. For example, certain TZDs have been reported to ameliorate type II diabetes by binding and activating PPARs (peroxisome proliferator-activated receptors). Nonetheless, no information is available on the interaction between the heterocyclic 2, 4-thiazolidinedione (2,4-TZD) moiety and serum albumin, which could affect the pharmacokinetics and pharmacodynamics of TZDs. In this study, we investigated the binding of 2,4-TZD to human serum albumin (HSA). Intrinsic fluorescence spectroscopy revealed a 1:1 binding stoichiometry between 2,4-TZD and HSA with a binding constant (Kb) of 1.69 ± 0.15 × 103 M−1 at 298 K. Isothermal titration calorimetry studies showed that 2,4-TZD/HSA binding was an exothermic and spontaneous reaction. Molecular docking analysis revealed that 2,4-TZD binds to HSA subdomain IB and that the complex formed is stabilized by van der Waal’s interactions and hydrogen bonds. Molecular dynamics simulation confirmed the stability of the HSA-TZD complex. Further, circular dichroism and 3D fluorescence studies showed that the global conformation of HSA was slightly altered by 2,4-TZD binding, enhancing its stability. The results obtained herein further help in understanding the pharmacokinetic properties of thiazolidinedione.

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Ortmeyer, Heidi K., Noni L. Bodkin, Joseph Haney, Shinji Yoshioka, Hiroyoshi Horikoshi y Barbara C. Hansen. "A Thiazolidinedione ImprovesIn VivoInsulin Action on Skeletal Muscle Glycogen Synthase in Insulin-Resistant Monkeys". International Journal of Experimental Diabetes Research 1, n.º 3 (2000): 195–202. http://dx.doi.org/10.1155/edr.2000.195.

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Thiazolidinediones (TZD) have been shown to have anti-diabetic effects including the ability to decrease fasting hyperglycemia and hyperinsulinemia, increase insulin-mediated glucose disposal rate (M) and decrease hepatic glucose production, but the mechanisms of action are not well established. To determine whether a TZD (R-102380, Sankyo Company Ltd., Tokyo, Japan) could improve insulin action on skeletal muscle glycogen synthase (GS), the rate-limiting enzyme in glycogen synthesis, 4 insulin-resistant obese monkeys were given I mg/kg/ day R-102380 p.o. for a 6-week period. Skeletal muscle GS activity and glucose 6-phosphate (G6P) content were compared between pre-dosing and dosing periods before and during the maximal insulin-stimulation of a euglycemic hyperinsulinemic clamp.Compared to pre-dosing, insulin-stimulated GS activity and G6P content were increased by this TZD: GS independent activity (p= 0.02), GS total activity (p= 0.005), GS fractional activity (p= 0.06) and G6P content (p= 0.02). The change in GS activity induced byin vivoinsulin (insulin-stimulated minus basal) was also increased by this TZD: GS independent activity (p= 0.03) and GS fractional activity (p= 0.04).We conclude that the TZD R-102380 improves insulin action at the skeletal muscle in part by increasing the activity of glycogen synthase. This improvement in insulin sensitivity may be a key factor in the anti-diabetic effect of the thiazolidinedione class of agents.

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Chis, Irina C., Doina Baltaru, Simona Clichici, Ovidiu Oniga, Ileana Cojocaru y Cristina Nastasa. "The Effects of a 5-Chromene-yl-thiazolidin-2,4-dione Derivative in Alleviating Oxidative Stress in Adjuvant-Induced Arthritis". Revista de Chimie 69, n.º 9 (15 de octubre de 2018): 2361–65. http://dx.doi.org/10.37358/rc.18.9.6534.

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Rheumatoid arthritis (RA) is a chronic inflammatory disease that reduces life quality and requires long-life therapy. Quercetin (Que) is a natural flavonoid with antioxidant and anti-inflammatory effects. (3-(2-(4-Chlorophenyl)-2-oxoethyl)-5-((6-methyl-4-oxo-4H-chromen-3-yl)methylene) thiazolidine-2,4-dione (TZD) is a thiazolidinedione derivative synthesized in our laboratory. This study was designed to investigate the antioxidant effects of the Que and TZD derivative administration in adjuvant-induced arthritic (AIA) rats. AIA was induced in Wistar rats by the intraplantar injection of Freund�s complete adjuvant (FCA), unilaterally in the right hind paw. The control non-arthritic rats and the arthritic rats were treated with Que (30 mg/kg/day) or TZD derivative (12 mg/kg/day) for 21 days. The antioxidant effects of 5-chromen-yl- thiazolidinedione were compared to Que. The serum levels of malondialdehyde (MDA) and protein carbonyl (PC) groups, the superoxide dismutase (SOD) and catalase (CAT) activity were assessed. AIA rats showed significatly increased oxidative stress parameter levels in the blood. The results indicated that the TZD derivative decreased the blood oxidative stress parameters in the treated arthritic rats, compared to Que. The antioxidant effects of 5-chromen-yl-thiazolidinedione in AIA suggest its therapeutic properties for the clinical treatment of RA.

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Kim, Won Jun, Jung Hyun Noh, Kyungdo Han y Cheol-Young Park. "The Association Between Second-Line Oral Antihyperglycemic Medication on Types of Dementia in Type 2 Diabetes: A Nationwide Real-World Longitudinal Study". Journal of Alzheimer's Disease 81, n.º 3 (1 de junio de 2021): 1263–72. http://dx.doi.org/10.3233/jad-201535.

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Background: There are few reports that evaluated the association between various types of dementia and dual oral therapy with antihyperglycemic medication. Objective: The goal of this study was to investigate the association between treatment of dual antihyperglycemic medication and dementia subclass in type 2 diabetes mellitus using the Korean National Health Insurance System. Methods: This study included 701,193 individuals with diabetes prescribed dual oral therapy between 2009 and 2012 from the Korean National Health Insurance Service Database, which were tracked until 2017. All-cause, Alzheimer’s (AD) and vascular dementia (VaD) were investigated by dual oral therapy. Adjustments were made for age, sex, income, diabetes duration, hypertension, dyslipidemia, smoking, drinking, exercise, body mass index, glucose level, and estimated glomerular filtration rate. Results: Dual therapy with metformin (Met) + dipeptidyl peptidase-4 inhibitor (DPP-4i), Met + thiazolidinedione (TZD), and sulfonylurea (SU) + thiazolidinediones (TZD) were significantly associated with all-cause dementia (HR = 0.904, 0.804, and 0.962, respectively) and VaD (HR = 0.865, 0.725, and 0.911, respectively), compared with Met + SU. Met + DPP-4i and Met + TZD were associated with significantly lower risk of AD (HR = 0.922 and 0.812), compared with Met + SU. Dual therapy with TZD was associated with a significantly lower risk of all-cause dementia, AD, and VaD than nonusers of TZD (HR = 0.918, 0.925 and 0.859, respectively). Conclusion: Adding TZD or DPP-4i instead of SU as second-line anti-diabetic treatment may be considered for delaying or preventing dementia. Also, TZD users relative to TZD non-users on dual oral therapy were significantly associated with lower risk of various types of dementia.

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Corigliano, Domenica M., Riyaz Syed, Sebastiano Messineo, Antonio Lupia, Rahul Patel, Chittireddy Venkata Ramana Reddy, Pramod K. Dubey et al. "Indole and 2,4-Thiazolidinedione conjugates as potential anticancer modulators". PeerJ 6 (8 de agosto de 2018): e5386. http://dx.doi.org/10.7717/peerj.5386.

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Background Thiazolidinediones (TZDs), also called glitazones, are five-membered carbon ring molecules commonly used for the management of insulin resistance and type 2 diabetes. Recently, many prospective studies have also documented the impact of these compounds as anti-proliferative agents, though several negative side effects such as hepatotoxicity, water retention and cardiac issues have been reported. In this work, we synthesized twenty-six new TZD analogues where the thiazolidinone moiety is directly connected to an N-heterocyclic ring in order to lower their toxic effects. Methods By adopting a widely applicable synthetic method, twenty-six TZD derivatives were synthesized and tested for their antiproliferative activity in MTT and Wound healing assays with PC3 (prostate cancer) and MCF-7 (breast cancer) cells. Results Three compounds, out of twenty-six, significantly decreased cellular viability and migration, and these effects were even more pronounced when compared with rosiglitazone, a well-known member of the TZD class of antidiabetic agents. As revealed by Western blot analysis, part of this antiproliferative effect was supported by apoptosis studies evaluating BCL-xL and C-PARP protein expression. Conclusion Our data highlight the promising potential of these TZD derivatives as anti-proliferative agents for the treatment of prostate and breast cancer.

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van de Vyver, M., E. Andrag, I. L. Cockburn y W. F. Ferris. "Thiazolidinedione-induced lipid droplet formation during osteogenic differentiation". Journal of Endocrinology 223, n.º 2 (10 de septiembre de 2014): 119–32. http://dx.doi.org/10.1530/joe-14-0425.

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Chronic administration of the insulin-sensitising drugs, thiazolidinediones (TZDs), results in low bone mineral density and ‘fatty bones’. This is thought to be due, at least in part, to aberrant differentiation of progenitor mesenchymal stem cells (MSCs) away from osteogenesis towards adipogenesis. This study directly compared the effects of rosiglitazone, pioglitazone, and netoglitazone treatment on osteogenesis and adipogenesis in MSCs derived from subcutaneous (SC) or visceral (PV) white adipose tissue. MSCs were isolated from adipose tissue depots of male Wistar rats and characterised using flow cytometry. The effects of TZD treatment on osteogenic and adipogenic differentiation were assessed histologically (day 14) and by quantitative PCR analysis (Pparγ2(Pparg2),Ap2(Fabp4), Adipsin(Adps),Msx2, Collagen I(Col1a1), andAlp) on days 0, 7, and 10. Uniquely, lipid droplet formation and mineralisation were found to occur concurrently in response to TZD treatment during osteogenesis. Compared with SC MSCs, PV MSCs were more prone to lipid accumulation under controlled osteogenic and adipogenic differentiation conditions. This study demonstrated that the extent of lipid accumulation is dependent on the nature of thePparligand and that SC and PV MSCs respond differently toin vitroTZD treatment, suggesting that metabolic status can contribute to the adverse effects associated with TZD treatment.

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Rosa, Fernanda, Misagh Moridi, Johan S. Osorio, Jayant Lohakare, Erminio Trevisi, Shelby Filley, Charles Estill y Massimo Bionaz. "2,4-Thiazolidinedione in Well-Fed Lactating Dairy Goats: II. Response to Intra-Mammary Infection". Veterinary Sciences 6, n.º 2 (5 de junio de 2019): 52. http://dx.doi.org/10.3390/vetsci6020052.

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In a prior experiment, treatment of goats with the putative PPARγ agonist 2,4-thiazolidinedione (2,4-TZD) ameliorated the response to intramammary infection without evidence of PPARγ activation. The lack of PPARγ activation was possibly due to deficiency of vitamin A and/or a poor body condition of the animals. Therefore, the present study hypothesized that activation of PPARγ by 2,4-TZD in goats supplemented with adequate amounts of vitamin A can improve the response to sub-clinical mastitis. Lactating goats receiving a diet that met National Research Council requirements, including vitamin A, were injected with 8 mg/kg BW of 2,4-TZD (n = 6) or saline (n = 6; control (CTR)) daily. Two weeks into treatment, all goats received Streptococcus uberis (IMI) in the right mammary gland. Blood biomarkers of metabolism, inflammation, and oxidative status plus leukocytes phagocytosis were measured. Mammary epithelial cells (MEC) and macrophages were isolated from milk and liver tissue collected for gene expression analysis. Milk fat was maintained by treatment with 2,4-TZD, but decreased in CTR, after IMI. Haptoglobin was increased after IMI only in 2,4-TZD without any effect on negative acute phase proteins, indicating an improved liver function. 2,4-TZD vs. CTR had a greater amount of globulin. The expression of inflammation-related genes was increased by IMI in both macrophages and MEC. Except for decreasing expression of SCD1 in MEC, 2,4-TZD did not affect the expression of measured genes. Results confirmed the successful induction of sub-clinical mastitis but did not confirm the positive effect of 2,4-TZD on the response to IMI in well-fed goats.

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Rosa, Fernanda, Johan S. Osorio, Erminio Trevisi, Francisco Yanqui-Rivera, Charles T. Estill y Massimo Bionaz. "2,4-Thiazolidinedione Treatment Improves the Innate Immune Response in Dairy Goats with Induced Subclinical Mastitis". PPAR Research 2017 (2017): 1–22. http://dx.doi.org/10.1155/2017/7097450.

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Mastitis is a major disease in dairy cows resulting in significant economic losses. In vitro works suggest that ruminants peroxisome proliferator-activated receptor gamma (PPARγ) can aid in improving the response to mastitis and can control milk fat synthesis. The objectives of the present experiment were to test if treatment with the putative PPARγ agonist 2,4-thiazolidinedione (TZD) improves (1) the response to subclinical mastitis and (2) milk fat production. Lactating goats received daily injections of 8 mg/kg BW of TZD or saline for 3 weeks. After one week of TZD injection, half of the goats in each group received intramammary infusion of Strep. uberis or saline in both halves for a total of 4 groups (n=6/group). TZD treatment did not affect milk fat but had positive effect on milk somatic cells count, blood nonesterified fatty acids, inflammatory markers, and liver function. TZD significantly increased myeloperoxidase but did not affect leukocytes phagocytosis or insulin. TZD increased adipocytes size and had minor effect on expression of PPARγ target genes in mammary epithelial cells but not in adipose tissue. Overall, TZD ameliorated the response to intramammary infection but the effect on milk fat synthesis and expression of related transcripts was less than expected.

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Govindarajan, R., E. R. Siegel, D. L. Simmons y N. P. Lang. "Thiazolidinedione (TZD) exposure and risk of squamous cell carcinoma of head and neck (SCCHN)". Journal of Clinical Oncology 25, n.º 18_suppl (20 de junio de 2007): 1511. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.1511.

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1511 Background: Peroxisome proliferator-activated receptor γ (PPARγ), a nucleic acid receptor, heterodimerizes with retinoic acid X receptor (RXR). Ligand activation of RXR leads to decreased proliferation of SCCHN cell lines. TZDs (syn: glitazones), used to treat diabetes mellitus (DM), are ligands for the RXR:PPARγ heterodimer. A retrospective study of diabetics attending the Veterans Affairs (VA) health care system was undertaken to assess the association between TZD exposure and the risk of developing SCCHN. Methods: Data were obtained from the electronic patient database VISN 16 (covering 10 VA institutions) for males aged ≥40 presenting with DM and no prior SCCHN between 10/01/96 and 12/31/03. DM and SCCHN diagnoses were identified using ICD9 codes. Subjects were followed until 12/31/05, and analyzed for SCCHN risk via Cox regression, using time-dependent covariates to model exposure to TZDs, insulin and other anti-DM agents. Results: 130,406 subjects met the study criteria. Median (quartiles) age at DM presentation was 64 (55–72).18.5% were African-American, 61.3% were Caucasian, and 20.2% were other/unknown. The table shows TZD exposure, SCCHN incidence and hazard ratios for SCCHN with exposure to TZD alone or in combination with insulin and other anti-DM agents after adjusting for age, race, BMI, and HbA1C. Conclusions: A 41%-55% reduction in the risk of SCCHN was observed in diabetic subjects treated with TZD alone, with insulin, and with other anti-DM agents. The decrease was statistically significant (P<0.05) for TZD alone and TZD with other agents, but not for TZD with insulin. These findings suggest a protective effect of TZD on the development of SCCHN. The mechanism is not clearly known but possibly mediated through RXR:PPARγ pathway. [Table: see text] No significant financial relationships to disclose.

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Klopper, Joshua P., Vibha Sharma, Reid Bissonnette y Bryan R. Haugen. "Combination PPARγand RXR Agonist Treatment in Melanoma Cells: Functional Importance of S100A2". PPAR Research 2010 (2010): 1–8. http://dx.doi.org/10.1155/2010/729876.

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Nuclear hormone receptors, including RXR and PPARγ, represent novel therapeutic targets in melanoma. We have previously shown that the DRO subline of the amelanotic melanoma A375 responds to rexinoid and thiazolidinedione (TZD) treatmentin vitroandin vivo. We performed microarray analysis of A375(DRO) after TZD and combination rexinoid/TZD treatment in which the calcium binding protein S100A2 had increased expression after rexinoid or TZD treatment and a synergistic increase to combination treatment. Increased S100A2 expression is dependent on an intact PPARγreceptor, but it is not sufficient to mediate the antiproliferative effects of rexinoid/TZD treatment. Over expression of S100A2 enhanced the effect of rexinoid and TZD treatment while inhibition of S100A2 expression attenuated the response to rexinoid/TZD treatment, suggesting that S100A2 is necessary for optimal response to RXR and PPARγactivation by respective ligands. In summary, we have identified potential downstream mediators of rexinoid and TZD treatment in a poorly differentiated melanoma and found that alterations in S100A2 expression affect RXR and PPARγsignaling in A375(DRO) cells. These studies provide insight into potential mechanisms of tumor response or resistance to these novel therapies.

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Más fuentes

Tesis sobre el tema "Thiazolidinedione (TZD)"

Spaeth, Brianne y Barbara Fontana. "A Cost-Effectiveness Analysis Comparing Glargine Versus Rosiglitazone or Pioglitazone for Patients Failing Metformin Plus a Sulfonylurea". The University of Arizona, 2008. http://hdl.handle.net/10150/624269.

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Class of 2008 Abstract
Objectives: To determine the cost-effectiveness of adding a thiazolidinedione (TZD) versus insulin glargine (glargine) as a triple regimen for treatment of Type 2 diabetes mellitus for patients not controlled with metformin and a sulfonylurea. Methods: A decision analytic model was developed to compare the clinical outcomes and costs of triple therapy with either a TZD or glargine. Published literature was used to determine treatment efficacy and the frequency of clinically important adverse effects. Cost data were obtained from the 2007 Physician Fee Reference and North Carolina Industrial Commission website. The decision tree was built using TreeAge software. Clinical outcome measures included HgA1c (A1C) control, hypoglycemia frequency, and the development of edema associated with the use of these medications. A Monte Carlo probabilistic sensitivity analysis was conducted to determine the mean and 95% CIs for both treatment efficacy and costs. Results: There was no statistically significant difference in the efficacy of adding either a TZD or glargine in achieving a goal A1C ≤ 7%. However, glargine triple therapy was estimated to be significantly less costly than TZD triple therapy ($3,161/yr; 95% CI $3,116 to $3,356 versus $3,769/yr; 95% CI $3,667 to $3,902, respectively). Conclusions: Most patients requiring triple therapy for the management of T2DM should receive glargine rather than a TZD due to the significantly lower cost producing similar clinical efficacy.

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Fulgencio, Jean-Pierre. "Effets d'un biguanide et de deux thiazolidinediones sur le métabolisme du glucose et des acides gras dans des hepatocytes de rat : des flux métaboliques à l'expression de gènes". Paris 7, 2003. http://www.theses.fr/2003PA077047.

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Capítulos de libros sobre el tema "Thiazolidinedione (TZD)"

Bourdon, Allen K., Greg Villareal, George Perry y Clyde F. Phelix. "Alzheimer's and Parkinson's Disease Novel Therapeutic Target". En Research Anthology on Diagnosing and Treating Neurocognitive Disorders, 411–26. IGI Global, 2021. http://dx.doi.org/10.4018/978-1-7998-3441-0.ch021.

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Thiazolidinedione (TZD) drugs (Takeda Pharmaceuticals and Metabolic Solutions Development Company) targeting inhibition of the mitochondrial pyruvate carrier (MPC) are currently being tested in clinical trials to prevent progression into mild cognitive impairment of Alzheimer's disease (AD) or in the pipeline to prevent neurodegeneration in Parkinson's disease (PD). These have Ki values in the µM range. This study was focused on identifying candidate drug precursors of the natural cinnamic acid products that might have good bioavailability in the nM ranges forming covalent thiol bonds with targets. In silico protein homology modeling and ligand docking has demonstrated that binding cysteine residues within the transport channel is a key part of the inhibitory mechanism. These are covalent thiohemiacetal bonds with the alpha-carbon, carboxylate group, off a phenol ring. Like the classic MPC inhibitors, these natural derivatives of hydroxycinnamic acid have a conjugated pi-system used to form thiol bonds with the cysteine residue via Michael addition.

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Seth, AK, DC Gajzer, P. Suwandhi, Y. Feng, S. Kato, C. Romero, R. Patel, Z. Rosenwaks, L. Poretsky y D. Seto-Young. "Thiazolidinediones (TZDs) Inhibit Bone Turnover." En The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego, P2–184—P2–184. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part2.p4.p2-184.

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Actas de conferencias sobre el tema "Thiazolidinedione (TZD)"

Synan, MJ, MD Burdick y RM Strieter. "Thiazolidinediones (TZDs) Inhibit the Expression of Pro-Angiogenic ELR+ CXC Chemokines in Non-Small Cell Lung Cancer (NSCLC) Cells Via a PPAR-γ Independent Mechanism." En American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5007.

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