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Relevant bibliographies by topics / Thiazolidinediones

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Academic literature on the topic 'Thiazolidinediones'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 March 2023

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Journal articles on the topic "Thiazolidinediones"

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Thangavel, Neelaveni, Mohammed Al Bratty, Sadique Akhtar Javed, Waquar Ahsan, and Hassan A. Alhazmi. "Targeting Peroxisome Proliferator-Activated Receptors Using Thiazolidinediones: Strategy for Design of Novel Antidiabetic Drugs." International Journal of Medicinal Chemistry 2017 (June 5, 2017): 1–20. http://dx.doi.org/10.1155/2017/1069718.

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Thiazolidinediones are a class of well-established antidiabetic drugs, also named as glitazones. Thiazolidinedione structure has been an important structural domain of research, involving design and development of new drugs for the treatment of type 2 diabetes. Extensive research on the mechanism of action and the structural requirements has revealed that the intended antidiabetic activity in type 2 diabetes is due to their agonistic effect on peroxisome proliferator-activated receptor (PPAR) belonging to the nuclear receptor super family. Glitazones have specific affinity to PPARγ, one of the subtypes of PPARs. Certain compounds under development have dual PPARα/γ agonistic activity which might be beneficial in obesity and diabetic cardiomyopathy. Interesting array of hybrid compounds of thiazolidinedione PPARγ agonists exhibited therapeutic potential beyond antidiabetic activity. Pharmacology and chemistry of thiazolidinediones as PPARγ agonists and the potential of newer analogues as dual agonists of PPARs and other emerging targets for the therapy of type 2 diabetes are presented. This review highlights the possible modifications of the structural components in the general frame work of thiazolidinediones with respect to their binding efficacy, potency, and selectivity which would guide the future research in design of novel thiazolidinedione derivatives for the management of type 2 diabetes.

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Arlt, W., P. Neogi, C. Gross, and WL Miller. "Cinnamic acid based thiazolidinediones inhibit human P450c17 and 3beta-hydroxysteroid dehydrogenase and improve insulin sensitivity independent of PPARgamma agonist activity." Journal of Molecular Endocrinology 32, no. 2 (April 1, 2004): 425–36. http://dx.doi.org/10.1677/jme.0.0320425.

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Thiazolidinediones improve insulin sensitivity in type 2 diabetes mellitus by acting as peroxisome proliferator-associated receptor gamma (PPARgamma) agonists, and decrease circulating androgen concentrations in polycystic ovary syndrome by unknown mechanisms. Some thiazolidinediones directly inhibit the steroidogenic enzymes P450c17 and 3beta-hydroxysteroid dehydrogenase type II (3betaHSDII) by distinct mechanisms. We synthesized five novel thiazolidinediones, CLX-M1 to -M5 by linking a 2,4-thiazolidinedione moiety to a substituted alpha-phenyl cinnamic acid previously shown to have glucose-lowering effects. Using yeast microsomes expressing human P450c17 and 3betaHSDII we found that cinnamic acid methyl esters with a double bond in the thiazolidinedione core structure (M3, M5) were stronger inhibitors of P450c17 than methyl esters with the conventional core (M1, M4). These four compounds inhibited 3betaHSDII equally well, while the free cinnamic acid analog (M2) did not inhibit either enzyme. Thus, the inhibition of P450c17 and 3betaHSDII by these novel thiazolidinediones reveals structure-activity relationships independent of PPARgamma transactivation. PPARgamma transactivation was moderate (M1), weak (M2, M3) or even absent (M4, M5). While the PPARgamma agonist activity of M1 was only 3% of that of rosiglitazone, both increased glucose uptake by 3T3-L1 adipocytes and reduced serum glucose levels in ob/ob and db/db mice to a similar extent. The similar glucose-lowering effects of M1 and rosiglitazone, despite their vast differences in PPARgamma agonist activity, suggests these two actions may occur by separate mechanisms.

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Singh Sethi, Navjot, Dn Prasad, Deepak Bhagwat, Anuradha Kumari, Madhu Sharma, and Sangeeta Kaundal. "SYNTHESIS, SPECTRAL, AND PHARMACOLOGICAL EVALUATION OF 3 AND 5 SUBSTITUTED 2,4-THIAZOLIDINEDIONE DERIVATIVES." Asian Journal of Pharmaceutical and Clinical Research 11, no. 11 (November 7, 2018): 363. http://dx.doi.org/10.22159/ajpcr.2018.v11i11.12008.

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Background: 2,4-Thiazolidinedione derivatives was launched as antidiabetics in 90’s. Later the derivatives of 2,4-thiazolidinedione were banned due to hepatotoxicity. To the date, much research has been directed toward the synthesis and novel uses of 2,4-thiazolidinedione compounds.Aim: The aim of the present study is to synthesize a set of 3,5-disudstituted-2,4-thiazolidinediones as antimicrobial. These compounds were evaluated for their antimicrobial activity.Method: First, the 2,4-thiazolidinedione was substituted at the position of 3 using sodium hydroxide and ethanol and then substituted at the position of 5 in the presence of piperdine by the Knoevenagel condensation method. The structures of the compounds were established on the basis of infrared and nuclear magnetic resonance spectral studies.Result: 3,5-disubstituted-5-benzylidine-2,4-thiazolidinediones derivative was synthesized using benzyl halides and aromatic aldehydes. The results obtained showed that TZ-1 exhibited good activity against Bacillus subtilis while no activity against Escherichia coli.Conclusion: Attachment of more heterocyclic rings containing Nitrogen on the 3rd position of 2,4-thiazolidinedione can enhance the antimicrobial activity. Addition of more lipophilic agents may increase the bioavailability and efficacy of the drug. Long alkyl chains on the benzylidene ring can also increase the lipophilic character, and further attachment of these kind of agents on benzylidene chain may produce safe and effective compounds in future.

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Chawla, P., Garg P, Panjwani D, and S. A. Saraf. "Synthesis of Some Novel 5-Substituted Arylidene – 2, 4 –Thiazolidinediones as Bioactive Agents." International Journal of Pharmaceutical Sciences and Nanotechnology 4, no. 1 (May 31, 2011): 1373–78. http://dx.doi.org/10.37285/ijpsn.2011.4.1.10.

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A series of 5-substituted arylidine-2, 4-thiazolidinediones derivatives were synthesized from 2, 4-thiazolidinedione and substituted aromatic aldehydes. The synthesized title compounds were screened for their in-vivo anti-inflammatory and analgesic and in-vitro antioxidant activities as per standard protocols. All the compounds were found to possess significant activities

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Bloomgarden, Z. T. "Thiazolidinediones." Diabetes Care 28, no. 2 (January 27, 2005): 488–93. http://dx.doi.org/10.2337/diacare.28.2.488.

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Grubb, Derek, JR Greenfield, and DJ Chisholm. "Thiazolidinediones." Australian Prescriber 27, no. 6 (December 1, 2004): 138–41. http://dx.doi.org/10.18773/austprescr.2004.114.

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Reynolds, Kathryn, and Ronald B. Goldberg. "Thiazolidinediones." Treatments in Endocrinology 5, no. 1 (2006): 25–36. http://dx.doi.org/10.2165/00024677-200605010-00004.

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Yki-Järvinen, Hannele. "Thiazolidinediones." New England Journal of Medicine 351, no. 11 (September 9, 2004): 1106–18. http://dx.doi.org/10.1056/nejmra041001.

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Henry, Robert R. "THIAZOLIDINEDIONES." Endocrinology and Metabolism Clinics of North America 26, no. 3 (September 1997): 553–73. http://dx.doi.org/10.1016/s0889-8529(05)70267-x.

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Owens, David R. "Thiazolidinediones." Clinical Drug Investigation 22, no. 8 (2002): 485–505. http://dx.doi.org/10.2165/00044011-200222080-00001.

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Dissertations / Theses on the topic "Thiazolidinediones"

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Shiau, Chung-Wai. "Thiazolidinediones: from peroxisome-proliferator-activated receptor γ(PPARγ) to anticancer agents." The Ohio State University, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=osu1128111032.

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Wei, Shuo. "Peroxisome Proliferator-Activated Receptor γ (PPARγ)-Independent Antitumor Effect of Thiazolidinediones." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1259167390.

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Shiau, Chung-Wai. "Thiazolidinediones: from peroxisome-proliferator-activated receptor [gamma] (PPAR[gamma]) to anticancer agents." Columbus, Ohio : Ohio State University, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1128111032.

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Leblond, Julie. "Utilisation des thiazolidinediones chez les patients atteints de diabète de type 2." Mémoire, Université de Sherbrooke, 2003. http://savoirs.usherbrooke.ca/handle/11143/3351.

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Le diabète est une maladie importante, tant en raison du nombre de personnes atteintes qu'en raison des diverses répercussions cliniques et économiques. En 2000, une nouvelle classe d'agents antidiabétiques, les thiazolidinediones, a été ajoutée à l'arsenal thérapeutique du diabète au Canada. Actuellement, la plupart des informations disponibles sur ces molécules proviennent d'études cliniques et très peu d'études de population ont été réalisées sur le sujet. Toutefois, nous savons que l'utilisation des médicaments dans la réalité est typiquement différente de celle des études cliniques randomisées. Si l'utilisation de ces médicaments s'avérait inadéquate, des coûts élevés pourraient y être associés. Les objectifs de cette étude étaient de décrire l'adhérence, ainsi que la persistance au traitement avec les thiazolidinediones et d'identifier ses déterminants. Des données démographiques, médicales et pharmaceutiques ont été obtenues à partir des banques de données de la Régie de l'assurance maladie du Québec. Les patients inclus dans cette étude ont été identifiés, entre octobre 2000 et juillet 2002, par une première prescription dispensée (nommée date index) de thiazolidinediones, pour un suivi variant de 1 à 22 mois. Les patients qui n'étaient pas inscrits à l'assurance médicament au moins un an avant la date index étaient exclus de la cohorte, tout comme les patients ayant été hospitalisés 30 jours et plus durant la période de suivi. Le renouvellement des thiazolidinediones sans interruption durant la période de suivi définissait la persistance au traitement et l'adhérence était déterminée comme étant la prise de 80% à 120% de la médication antidiabétique prescrite. Le taux de persistance a été estimé à l'aide d'une analyse de Kaplan-Meier et les déterminants de la persistance ont été identifiés avec un modèle de Cox."--Résumé abrégé par UMI.

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Botton, Thomas. "Étude des effets anti-mélanome des thiazolidinediones : implication de la chimiokine CXCL1." Nice, 2010. http://www.theses.fr/2010NICE4028.

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Les thiazolidinediones (TZD) sont utilisés dans le traitement du diabète de type 2. Cependant, des études ont montré que les TZD inhibent la croissance de nombreuses cellules tumorales. Nous avons donc testé les effets des TZD dans la lutte contre le mélanome, un cancer très agressif contre lequel on ne dispose d’aucun traitement efficace au stade métastatique. Nous avons montré qu’un TZD, la ciglitazone, inhibe la prolifération des cellules de mélanome mais pas celle des mélanocytes. A de faibles doses, la ciglitazone induit un arrêt du cycle alors qu’à de fortes doses elle entraine une apoptose. Les effets antinéoplasiques de la ciglitazone ont été confirmés dans un modèle murin de xénogreffe de mélanome. Nous avons alors montré que les effets biologiques de la ciglitazone sont précédés par une forte diminution de CXCL1, une chimiokine oncogénique surexprimée durant la mélanomagenèse. Cette diminution de CXCL1 est associée à une diminution de MITF, un facteur de transcription contrôlant à la fois la différenciation mélanocytaire et la progression tumorale des cellules de mélanome. Des expériences de xénogreffe ont confirmé que la diminution du potentiel tumoral des cellules de mélanome est associée à une inhibition de l’expression de MITF et du taux sérique de CXCL1 dans les souris traitées à la ciglitazone. Nos travaux suggèrent donc que la ciglitazone pourrait être un candidat intéressant pour la mise en place d’un test clinique. Ils démontrent également l’existence d’un axe MITF/CXCL1 qui semble jouer un rôle clé dans la tumorogénicité des cellules de mélanome. Cet axe pourrait constituer une cible thérapeutique intéressante dans la lutte contre le mélanome
Thiazolidinediones (TZD) are commonly used in the treatment of type 2 diabetes. However, studies on various cancer types have shown that TZD inhibit tumor growth. Thus, we have tested the effects of TZD in the struggle against melanoma, a very aggressive cancer for which there is no hitherto efficient therapeutics when it is metastatic. We have shown in vitro that ciglitazone, a member of the TZD family, is able to inhibit proliferation of melanoma cells but not of melanocytes. At low concentrations, ciglitazone effects on melanoma cells are mediated by a cell cycle arrest while higher concentrations induce cell death by apoptosis. Then, antineoplastic effects of ciglitazone have been confirmed in a xenograft model. Next, we have shown that the biological effects of ciglitazone are preceded by a dramatic decrease in CXCL1. This chemokine overexpressed in melanoma contributes to tumorigenicity. Interestingly, ciglitazone-induced CXCL1 decrease is mediated by the downregulation of microphthalmia-associated transcription factor, MITF, the master gene in melanocyte differentiation and involved in melanoma development. Additional xenograft experiments have emphasized that dramatic decrease in melanoma tumor potential was associated with an inhibition of MITF and a decrease in serum CXCL1 levels of ciglitazone-treated mice. Thus, our results suggest that ciglitazone might be an interesting candidate for clinical trial in melanoma treatment. They also demonstrate existence of a MITF/CXCL1 axis and highlight the key role of this specific pathway in melanoma malignancy. This axis could be a potential interesting therapeutic target in the future of the struggle against melanoma

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Leblond, Julie. "Utilisations des thiazolidinediones chez les patients atteints de diabète de type 2." Sherbrooke : Université de Sherbrooke, 2003.

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Lima, José Gildo de. "Thiazolidinediones et imidazolidinediones substituées : synthèse, stucture, étude pharmacologique et relations quantitatives structure-activité." Université Joseph Fourier (Grenoble), 1992. http://www.theses.fr/1992GRE18009.

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Fadnavis, Rucha. "Effect of hyperglycemia and thiazolidinediones on cardiac angiotensin converting enzyme 2 (ACE2) and neprilysin (NEP) in db/db diabetic mice." Wright State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=wright1503958100026796.

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Colin-Cassin, Christelle. "Activité PPARgamma-indépendante des ligands de PPAR gamma : une piste pour le traitement des cancers du sein ?" Thesis, Université de Lorraine, 2013. http://www.theses.fr/2013LORR0232/document.

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L'un des enjeux majeurs de la recherche anti-cancéreuse est de développer de nouvelles thérapies en direction des tumeurs réfractaires aux traitements conventionnels. Dans ce contexte, l'identification récente de l'activité anti-tumorale PPARgamma-indépendante des thiazolidinediones ouvre de nouvelles perspectives thérapeutiques. Au sein du laboratoire, il a été montré qu'un analogue inactif de la TGZ, la delta2-TGZ, induit une dégradation protéasome-dépendante du récepteur alpha aux oestrogènes de manière PPARgamma-indépendante. A partir de ces données, les objectifs de ma thèse ont été 1) de participer à la caractérisation de nouveaux composés à activité anti-cancéreuse 2) de mieux comprendre les mécanismes PPARgamma-indépendants mis en jeu dans l'effet anti-cancéreux des TZD. Lors de ce travail de thèse, nous avons caractérisé de nouveaux composés plus efficaces que la delta2-TGZ pour l'inhibition de la prolifération des cellules cancéreuses mammaires MCF-7 et MDA-MB-231 et faiblement toxiques sur des cultures primaires d'hépatocytes humains. De plus, nous avons montré que la delta2-TGZ est capable d'induire un stress du réticulum endoplasmique à des temps précoces dès 3 heures et une apoptose à des temps plus tardifs 48 heures. Cependant, nous n'avons pas pu conclure à l'existence d'un lien entre les deux mécanismes. Enfin, nous avons montré que la biotinylation d'un ligand naturel de PPARgamma, la 15d-PGJ2, accroît son effet anti-prolifératif sur les cellules cancéreuses mammaires MCF-7 et MDA-MB-231 et conduit à un stress du réticulum endoplasmique et à une mort par apoptose. Ces effets sont partiellement dépendants de PPARgamma pour le stress du réticulum endoplasmique mais strictement PPARgamma-indépendants pour l'apoptose. Ce travail pourrait permettre de constituer de nouveaux outils thérapeutiques dans le traitement du cancer du sein
One of the main goals of the anti-cancer research is to develop new therapeutic option for resistant tumor. In this context, the recent discovery of thiazolidinedione devoid of PPARgamma activity with a strong anti-cancer effect opens new perspectives. In a previous study, the laboratory showed that an inactive derivative of PPARgamma, the delta2-TGZ, induce a proteasome-dependent degradation of estrogen receptor alpha in PPARgamma-independent way. Thus, during my thesis we aimed 1) to participate in the study of new compounds less toxic and more effective to inhibit the proliferation of mammary cancer cells, 2) to better understand PPARgamma-independent mechanisms involved in the anti-cancer effect of the TZD. In the present work, we characterise new compounds more effective than delta2-TGZ to inhibit the proliferation of the breast cancer cells MCF-7 and MDA-MB-231 and are less toxic on primary culture of human hepatocytes. We pursued the study on mechanisms involved in PPARgamma-independent anti-proliferative activity of delta2-TGZ. We showed that delta2-TGZ is able to induce endoplasmic reticulum stress as soon as 3 hours and apoptosis in later times 48 hours of treatment. Nevertheless we could not conclude of the existence of a link between these two pathways. Finally, we studied the effect of the biotinylation of a natural ligand of PPAR?: the 15d-PGJ2. This modification drive to an increased effect of the 15d-PGJ2 on the anti-proliferative effect of breast cancer cells, reticulum endoplasmic stress and death by apoptosis. These effects are partially PPARgamma-dependent for reticulum endoplasmic stress and only PPARgamma-independent for apoptosis. This work highlighted new promising tools of breast cancers treatment

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Geoffroy, Marine. "Rôle de la claudine 1 dans les cellules cancéreuses mammaires triple-négatives et son implication dans les effets anticancéreux de dérivés de la troglitazone." Thesis, Université de Lorraine, 2018. http://www.theses.fr/2018LORR0056/document.

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Un défi majeur en cancérologie est le traitement des tumeurs mammaires dites triple-négatives (ER-, PR-, HER2-). Elles sont le plus souvent résistantes aux traitements conventionnels et présentent un haut risque de récidive. De plus, l’absence de cibles thérapeutiques ne permet pas le développement de thérapie spécifique. 78% de ces tumeurs expriment faiblement la claudine 1 et sont de très mauvais pronostic. Cette protéine est impliquée dans l'adhérence des cellules entre elles et pourrait jouer un rôle suppresseur de tumeur dans les cancers mammaires. Dans ce contexte, nous étudions si sa réexpression pourrait être une piste de traitement. Au laboratoire, nous avons développé des dérivés de la famille des thiazolidinediones (TZD) qui stimulent l’expression de la claudine 1 et induisent l’apoptose des cellules cancéreuses mammaires. Les objectifs de ma thèse ont consisté 1) à déterminer l’implication de la claudine 1 dans l’effet pro-apoptotique de ces composés 2) à l’étude de leurs mécanismes d’action 3) évaluer si l’expression de la claudine 1 pourrait sensibiliser les cellules cancéreuses triple-négatives aux agents de chimiothérapie. Au cours de cette thèse, nous avons montré que la surexpression de la claudine 1 et le composé Δ2-TGZ induisent l’apoptose des cellules triple-négatives « claudin 1-low » MDA-MB-231 et Hs578T. De plus, la claudine 1 est impliquée dans l’effet pro-apoptotique de la Δ2-TGZ dans les cellules MDA-MB-231. Par ailleurs, nous avons démontré que les dérivés TGZ, la Δ2-TGZ et l’AB186, agissent de manière précoce en modifiant la morphologie des cellules suivie d’une réexpression de la claudine 1 membranaire et d’une inhibition de la migration cellulaire avant même d’induire la mort cellulaire par apoptose. De plus, la surexpression de la claudine 1 inhibe la migration cellulaire associée à la perte des fibres de stress et la formation des jonctions intercellulaires. Nous avons également montré que la réexpression de la claudine 1 sensibilise les cellules MDA-MB-231 à l’agent de chimiothérapie, le 5-FU. L’ensemble des résultats de thèse a permis de mieux comprendre le mécanisme d’action de la Δ2-TGZ et de l’AB186 sur les cellules cancéreuses mammaires mais aussi d’identifier la claudine 1 comme cible potentielle prometteuse dans les cellules triple-négatives « claudin 1-low »
A major challenge in oncology is the treatment of triple-negative breast cancer (ER-, PR-, HER2-) as no targeted therapy are available. These tumors present often a chemotherapy resistance and a higher relapse incidence. 78% of them do not express claudin 1 and display a poor prognosis. Claudin 1 is involved in cell-cell adhesion and may be a tumor suppressor gene in breast cancer. In this context, we study if claudin 1 re-expression could be a possible approach. In the laboratory, we developed derivatives thaziolidinediones (TZD) compounds, which increase claudin 1 expression and lead to apoptosis of breast cancer cells. The goals of my thesis is 1) to characterize the involvement of claudin 1 in their pro-apoptotic effect 2) to study their mechanism of action 3) to determine if claudin 1 could sensitize the TNBC cells to the chemotherapy agents. During my thesis, we showed that claudin 1 overexpression and the compound Δ2-TGZ induce apoptosis of TNBC « claudin 1-low » MDA-MB-231 and Hs578T cells. Claudin 1 is involved in the pro-apoptotic effect of Δ2-TGZ in MDA-MB-231 cells. Then, we demonstrated that Δ2-TGZ and AB186 lead to early action through a modification of cell morphology followed an expression of claudin 1 at the membrane and an inhibition of cell migration before the apoptosis process. In addition, claudin 1 overexpression decreases the cell migration through the loss of stress fibers and the formation of cell junctions. We showed that claudin 1 overexpression potentialize the pro-apoptotic effect of Δ2-TGZ in MDA-MB-231 cells. Finally, we observed that claudin 1 sensitize the MDA-MB-231 cells to 5-FU. In fine, our data allowed a better understanding of Δ2-TGZ and AB186 mechanism of action and identification of claudin 1 as a promising target in TNBC « claudin 1-low »

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Book chapters on the topic "Thiazolidinediones"

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Won, Jong Chul. "Thiazolidinediones (TZDs)." In Stroke Revisited, 131–41. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-5123-6_11.

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Suvag, Seda, Kristina M. Utzschneider, and Steven E. Kahn. "Treatment with Thiazolidinediones." In The Metabolic Syndrome, 117–46. Vienna: Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1331-8_9.

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Maroo, Anjli, and W. H. Wilson Tang. "Effects of Thiazolidinediones on Serum Lipoproteins." In Therapeutic Lipidology, 149–58. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-533-6_8.

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Doustkhah, Esmail, and Fatemeh Majidi Arlan. "Synthesis of Bioactive Thioxoimidazolidinones, Oxazolidinones, Thioxothiazolidinones, Thiazolidinediones." In N-Heterocycles, 443–59. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-0832-3_13.

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Khamaisi, M., L. Symmer, and I. Raz. "Thiazolidinediones in Cardiovascular Risk in Type 2 Diabetes Mellitus." In Cardiovascular Risk in Type 2 Diabetes Mellitus, 193–203. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-59352-9_17.

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Horton, Edward S., A. Enrique Caballero, Rola Saouaf, and Aristidis Veves. "Effects of Thiazolidinediones on Vascular Reactivity and Endothelial Dysfunction." In Medical Science Symposia Series, 35–40. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1171-7_6.

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Siddiqui, Mohammad S., and Arun J. Sanyal. "Drug Therapy for NASH: Insulin-Sensitizing Agents (Metformin and Thiazolidinediones)." In Non-Alcoholic Fatty Liver Disease, 271–83. Oxford, UK: Wiley-Blackwell, 2013. http://dx.doi.org/10.1002/9781118556153.ch24.

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Taskinen, Marja-Riitta. "Are Thiazolidinediones Superior to Standard Therapy in the Treatment of Type 2 Diabetes?" In Medical Science Symposia Series, 149–55. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1171-7_21.

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Glandt, Mariela, and Zachary Bloomgarden. "Da Qing, Finnish DPP, Tripod, and Dream: Lifestyle and Thiazolidinediones in the Prevention of Diabetes." In Prevention of Type 2 Diabetes, 189–202. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3314-9_11.

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Yamada, Daishiro, Ken Kato, Sanae Midorikawa, Wakano Satoh, Shigeatsu Hashimoto, Hiroaki Satoh, Kazuhisa Tsukamoto, and Tsuyoshi Watanabe. "Improvement by Thiazolidinediones of Vascular Endothelial Cell Dysfunction in Diabetic Patients: A Possible New Physiological Role of PPARγ." In Lipoprotein Metabolism and Atherogenesis, 71–73. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-68424-4_16.

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Conference papers on the topic "Thiazolidinediones"

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Ivankin, Dmitry, Alexandra Zakharenko, Olga Luzina, Olga Lavrik, and Nariman Salakhutdinov. "Synthesis of novel TDP1 inhibitors – thiazolidinones, thiazolidinediones containing terpenoid substituents." In 7th International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2021. http://dx.doi.org/10.3390/ecmc2021-11393.

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Koga, Hironori, Karuppaiyah Selvendiran, Ramadoss Sivakumar, Takafumi Yoshida, Takuji Torimura, Takato Ueno, and Michio Sata. "Abstract 2746: Thiazolidinediones augment anticancer effects of gemcitabine on human pancreatic cancer cells through PPARδ activation." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2746.

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Tan, X., and JE Ward. "Thiazolidinediones Inhibit TGFβ-Mediated Epithelial Mesenchymal Transition of A549 Cells Via PPARγ Dependent and Independent Pathways." In 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.a5300.

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Synan, MJ, MD Burdick, and 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." In 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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Zaghloul, Nancy, Ahmed Awaisu, Ahmed Mahfouz, Sumaya Al Saadi, and Hazem Elewa. "Trends of use of SGLT2 inhibitors in Qatar." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0108.

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Abstract:

Background: Type 2 diabetes mellitus (T2DM) represents a growing health challenge in Qatar and worldwide. T2DM is associated with a high risk of cardiovascular (CV) morbidity and mortality, and progression of renal disease. Sodium glucose co-transporter 2 inhibitors (SGLT2is) are the most recently approved class of glucose lowering medications (GLMs). To date, there is a limited knowledge about the adoption of SGLT2is by clinicians compared to other oral GLMs in Qatar and Middle East and North Africa (MENA) region. Accordingly, this proposed study aims to explore the trends in SGLT2is use compared to other oral GLMs in Qatar from 2016 to 2020. Methods: This is a descriptive, retrospective cross-sectional study where information on all oral GLMs prescriptions dispensed as in- or out-patient from 2016 to 2020 in all Hamad Medical Corporation (HMC) hospitals were collected. Outcomes included the number and relative frequency of quarterly prescriptions of different oral GLMs classes [metformin, sulfonylureas (SUs), dipeptidyl peptidase 4 inhibitors (DPP-4is), thiazolidinediones (TZDs), meglitinides (MEGs), α-glucosidase inhibitors (AGIs), and SGLT2is] from 2016 to 2020. Results: Overall, the prescription rate of GLMs increased during the last five years. SGLT2is use increased over the years after being introduced to the formulary in 2017, replacing SUs which exhibited significant decline between 2017 and 2020. There was a slight reduction in metformin use, and a slight increase in DPP-4is use. TZDs, MEGs, and AGIs prescriptions remained stable. Among SGLT2is, empagliflozin showed considerable increase on the expense of dapagliflozin which decreased significantly by the end of 2018. Conclusion: SGLT2is have been gradually replacing SUs in Qatar and the trend of their use is similar to that reported in other countries. The trend among SGLT2is suggests greater preference for empagliflozin over dapagliflozin.

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Lončarić, Melita, Maja Molnar, Ivica Strelec, and Valentina Pavić. "Synthesis of thiazolidinedione derivatives and their lipoxygenase inhibition." In 7th International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2021. http://dx.doi.org/10.3390/ecmc2021-11478.

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Uray, Iván P., Jennifer M. Rodenberg, Yun Zhang, Jamal L. Hill, and Powel H. Brown. "Abstract 2804: The thiazolidinedione pioglitazone enhances the cancer preventive activity of the rexinoid LG100268 in Her2/neu induced breast cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2804.

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Davies, GF, AR Ross, BH Juurlink, and HA Troy. "The thiazolidinedione peroxisome proliferator-activated receptor gamma (PPARγ) agonist troglitazone alters histone post-translational modifications in MCF7 breast cancer cells." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-2140.

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Velayudhan, Jyoti, Aaron C. Haran, and Cliff D. Wright. "The Non-Thiazolidinedione PPAR-Gamma Ligand, GW1929 Displays Anti-Inflammatory Activity In Poly (I:C)-Induced Air-Liquid Interface Human Bronchial Epithelial Cells." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2827.

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