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Journal articles on the topic 'Thiazolidinediones'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 March 2023

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

OVALLE, FERNANDO, and J. FERNANDO OVALLE-BERÚMEN. "Thiazolidinediones." Southern Medical Journal 95, no. 10 (October 2002): 1188–94. http://dx.doi.org/10.1097/00007611-200210000-00016.

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12

OVALLE, FERNANDO, and FERNANDO J. OVALLE-BERUMEN. "Thiazolidinediones." Southern Medical Journal 95, no. 10 (October 2002): 1188–94. http://dx.doi.org/10.1097/00007611-200295100-00017.

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13

Filisola-Villaseñor, Jessica Georgina, María E. Aranda-Barradas, Susana Patricia Miranda-Castro, Jessica Elena Mendieta-Wejebe, Amaranta Sarai Valdez Guerrero, Selene Amasis Guillen Castro, Macario Martínez Castillo, Feliciano Tamay-Cach, and Samuel Álvarez-Almazán. "Impact of Molecular Symmetry/Asymmetry on Insulin-Sensitizing Treatments for Type 2 Diabetes." Symmetry 14, no. 6 (June 15, 2022): 1240. http://dx.doi.org/10.3390/sym14061240.

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Although the advantages and disadvantages of asymmetrical thiazolidinediones as insulin-sensitizers have been well-studied, the relevance of symmetry and asymmetry for thiazolidinediones and biguanides has scarcely been explored. Regarding symmetrical molecules, only one thiazolidinedione and no biguanides have been evaluated and proposed as an antihyperglycemic agent for treating type 2 diabetes. Since molecular structure defines physicochemical, pharmacological, and toxicological properties, it is important to gain greater insights into poorly investigated patterns. For example, compounds with intrinsic antioxidant properties commonly have low toxicity. Additionally, the molecular symmetry and asymmetry of ligands are each associated with affinity for certain types of receptors. An advantageous response obtained in one therapeutic application may imply a poor or even adverse effect in another. Within the context of general patterns, each compound must be assessed individually. The current review aimed to summarize the available evidence for the advantages and disadvantages of utilizing symmetrical and asymmetrical thiazolidinediones and biguanides as insulin sensitizers in patients with type 2 diabetes. Other applications of these same compounds are also examined as well as the various uses of additional symmetrical molecules. More research is needed to exploit the potential of symmetrical molecules as insulin sensitizers.

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14

Zhang, Yuliang, and Zhongqiang Zhou. "A Solvent-Free Protocol for the Green Synthesis of 5-Arylidene-2,4-thiazolidinediones Using Ethylenediamine Diacetate as Catalyst." Organic Chemistry International 2012 (September 2, 2012): 1–5. http://dx.doi.org/10.1155/2012/194784.

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A simple and efficient synthesis of 5-arylidene-2,4-thiazolidinediones by the Knoevenagel condensation of aromatic aldehydes with 2,4-thiazolidinedione catalyzed by ethylenediamine diacetate under solvent-free conditions is described. The major advantages of this method are simple experimental and work-up procedures, solvent-free reaction conditions, small amount of catalyst, short reaction time, high yields, and utilization of an inexpensive and reusable catalyst.

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15

Bireddy, Srinivasa Reddy, Veera Swamy Konkala, Chandraiah Godugu, and Pramod Kumar Dubey. "A Review on the Synthesis and Biological Studies of 2,4-Thiazolidinedione Derivatives." Mini-Reviews in Organic Chemistry 17, no. 8 (December 24, 2020): 958–74. http://dx.doi.org/10.2174/1570193x17666200221123633.

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2,4-Thiazolidinediones are versatile scaffolds with a unique structural feature of hydrogen bonding donor and the hydrogen bonding acceptor region. This review deals with the synthesis of various bio-active 2,4-thiazolidinedione derivatives. It is presented on the basis of the linker variations at 3rd & 5th positions of 2,4-thizolidinediones. Biological evaluations of various derivatives thus prepared and toxicity studies on the respective products as given by various researchers/ Research groups have been described.

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16

Damkaci, Fehmi, Adam A. Szymaniak, Jason P. Biasini, and Ryan Cotroneo. "Synthesis of Thiazolidinedione Compound Library." Compounds 2, no. 3 (July 5, 2022): 182–90. http://dx.doi.org/10.3390/compounds2030013.

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Thiazolidinediones (TZDs), also known as Glitazones, have anti-diabetic, anti-inflammatory and anti-cancer properties. A simple, efficient and cost-effective synthesis of a thiazolidinedione compound library was developed. The synthesis is facilitated by microwave irradiation in three of the four steps followed by reduction under pressurized hydrogen gas using palladium hydroxide. All reactions, except one, were completed within an hour and provided desired products in moderate to good yields after a simple work-up.

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17

Colca, Jerry R., William G. McDonald, Daniel J. Waldon, Joseph W. Leone, June M. Lull, Carol A. Bannow, Eric T. Lund, and W. Rodney Mathews. "Identification of a novel mitochondrial protein (“mitoNEET”) cross-linked specifically by a thiazolidinedione photoprobe." American Journal of Physiology-Endocrinology and Metabolism 286, no. 2 (February 2004): E252—E260. http://dx.doi.org/10.1152/ajpendo.00424.2003.

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Thiazolidinediones address underlying causes of type 2 diabetes, although their mechanism of action is not clearly understood. The compounds are thought to function as direct activators of the nuclear receptor PPARγ (peroxisome proliferator-activated receptor-γ), although pioglitazone, the weaker agonist of the two thiazolidinediones now in clinical use, seems to have more useful effects on circulating lipids. We have used tritiated pioglitazone and a photoaffinity cross-linker to identify a novel binding site in mitochondria. A saturable binding site for [3H]pioglitazone was solubilized from the membranes with CHAPS and migrated as a large complex by size exclusion chromatography. The binding correlated with a <17-kDa protein (m17), marked by a photoaffinity cross-linker, in both subcellular location and selectivity of competition by analogs. The protein was isolated and identified by mass spectrometry analysis and NH2-terminal sequencing. Three synthetic peptides with potential antigenic properties were synthesized from the predicted nontransmembrane sequence to generate antibodies in rabbits. Western blots show that this protein, which we have termed “mitoNEET,” is located in the mitochondrial fraction of rodent brain, liver, and skeletal muscle, showing the identical subcellular location and migration on SDS-PAGE as the protein cross-linked specifically by the thiazolidinedione photoprobe. The protein exists in low levels in preadipocytes, and expression increases exponentially in differentiated adipocytes. The synthetic protein bound to solid phase associated with a complex of solubilized mitochondrial proteins, including the trifunctional β-oxidation protein. It is possible that thiazolidinedione modification of the function of the mitochondrial target may contribute to lipid lowering and/or antidiabetic actions.

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18

Scheen, Andr?? J. "Hepatotoxicity with Thiazolidinediones." Drug Safety 24, no. 12 (2001): 873–88. http://dx.doi.org/10.2165/00002018-200124120-00002.

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19

Huang, Alvin, and Philip Raskin. "Thiazolidinediones and Insulin." Treatments in Endocrinology 4, no. 4 (2005): 205–20. http://dx.doi.org/10.2165/00024677-200504040-00002.

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20

Consoli, A., and E. Devangelio. "Thiazolidinediones and inflammation." Lupus 14, no. 9 (September 2005): 794–97. http://dx.doi.org/10.1191/0961203305lu2223oa.

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21

Isley, William L., and Julie C. Oki. "Hepatotoxicity of thiazolidinediones." Diabetes, Obesity and Metabolism 3, no. 6 (December 2001): 389–92. http://dx.doi.org/10.1046/j.1463-1326.2001.00159.x.

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22

Schoonjans, Kristina, and Johan Auwerx. "Thiazolidinediones: an update." Lancet 355, no. 9208 (March 2000): 1008–10. http://dx.doi.org/10.1016/s0140-6736(00)90002-3.

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23

Wolfe, Sidney M., Peter Lurie, Larry D. Sasich, and Elizabeth Barbehenn. "Information on thiazolidinediones." Lancet 356, no. 9225 (July 2000): 254–55. http://dx.doi.org/10.1016/s0140-6736(05)74507-4.

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24

Auwerx, Johan. "Information on thiazolidinediones." Lancet 356, no. 9225 (July 2000): 255. http://dx.doi.org/10.1016/s0140-6736(05)74508-6.

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25

Isley, William L. "Hepatotoxicity of thiazolidinediones." Expert Opinion on Drug Safety 2, no. 6 (November 2003): 581–86. http://dx.doi.org/10.1517/14740338.2.6.581.

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26

Boyd, Alan S. "Thiazolidinediones in dermatology." International Journal of Dermatology 46, no. 6 (June 2007): 557–63. http://dx.doi.org/10.1111/j.1365-4632.2007.03273.x.

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27

Bailey, Clifford J., and Caroline Day. "Review: Thiazolidinediones today." British Journal of Diabetes & Vascular Disease 1, no. 1 (August 2001): 7–13. http://dx.doi.org/10.1177/14746514010010010201.

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28

Schwab, A. M., S. Granholm, E. Persson, B. Wilkes, U. H. Lerner, and H. H. Conaway. "Stimulation of Resorption in Cultured Mouse Calvarial Bones by Thiazolidinediones." Endocrinology 146, no. 10 (October 1, 2005): 4349–61. http://dx.doi.org/10.1210/en.2005-0601.

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Dosage-dependent release of 45Ca was observed from prelabeled mouse calvarial bones after treatment with two thiazolidinediones, troglitazone and ciglitazone. Release of 45Ca by ciglitazone was decreased by the osteoclast inhibitors acetazolamide, calcitonin, 3-amino-1-hydroxypropylidene-1,1-bisphosphonate, and IL-4, but not affected by the peroxisome proliferator-activated receptor γ antagonist, GW 9662, the mitotic inhibitor, hydroxyurea, or indomethacin. Enhanced expression of receptor activator of nuclear factor-κB ligand (RANKL) mRNA and protein and decreased osteoprotegerin (OPG) mRNA and protein were noted after ciglitazone treatment of calvariae. Ciglitazone and RANKL each caused increased mRNA expression of osteoclast markers: calcitonin receptor, tartrate-resistant acid phosphatase, cathepsin K, matrix metalloproteinase-9, integrin β3, and nuclear factor of activated T cells 2. OPG inhibited mRNA expression of RANKL stimulated by ciglitazone, mRNA expression of osteoclast markers stimulated by ciglitazone and RANKL, and 45Ca release stimulated by troglitazone and ciglitazone. Increased expression of IL-1α mRNA by ciglitazone was not linked to resorption stimulated by the thiazolidinedione. Ciglitazone did not increase adipogenic gene expression but enhanced osteocalcin mRNA in calvariae. In addition to exhibiting sensitivity to OPG, data indicate that stimulation of osteoclast differentiation and activity by thiazolidinediones may occur by a nonperoxisome proliferator-activated receptor γ-dependent pathway that does not require cell proliferation, prostaglandins, or IL-1α but is characterized by an increased RANKL to OPG ratio.

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29

Mueller, Sarah L., Panagiotis K. Chrysanthopoulos, Maria A. Halili, Caryn Hepburn, Tom Nebl, Claudiu T. Supuran, Alessio Nocentini, Thomas S. Peat, and Sally-Ann Poulsen. "The Glitazone Class of Drugs as Carbonic Anhydrase Inhibitors—A Spin-Off Discovery from Fragment Screening." Molecules 26, no. 10 (May 18, 2021): 3010. http://dx.doi.org/10.3390/molecules26103010.

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The approved drugs that target carbonic anhydrases (CA, EC 4.2.1.1), a family of zinc metalloenzymes, comprise almost exclusively of primary sulfonamides (R-SO2NH2) as the zinc binding chemotype. New clinical applications for CA inhibitors, particularly for hard-to-treat cancers, has driven a growing interest in the development of novel CA inhibitors. We recently discovered that the thiazolidinedione heterocycle, where the ring nitrogen carries no substituent, is a new zinc binding group and an alternate CA inhibitor chemotype. This heterocycle is curiously also a substructure of the glitazone class of drugs used in the treatment options for type 2 diabetes. Herein, we investigate and characterise three glitazone drugs (troglitazone 11, rosiglitazone 12 and pioglitazone 13) for binding to CA using native mass spectrometry, protein X-ray crystallography and hydrogen–deuterium exchange (HDX) mass spectrometry, followed by CA enzyme inhibition studies. The glitazone drugs all displayed appreciable binding to and inhibition of CA isozymes. Given that thiazolidinediones are not credited as a zinc binding group nor known as CA inhibitors, our findings indicate that CA may be an off-target of these compounds when used clinically. Furthermore, thiazolidinediones may represent a new opportunity for the development of novel CA inhibitors as future drugs.

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30

Honisett, Suzy Y., Lily Stojanovska, Krishnankutty Sudhir, Bronwyn A. Kingwell, Tye Dawood, and Paul A. Komesaroff. "Hormone Therapy Impairs Endothelial Function in Postmenopausal Women with Type 2 Diabetes Mellitus Treated with Rosiglitazone." Journal of Clinical Endocrinology & Metabolism 89, no. 9 (September 1, 2004): 4615–19. http://dx.doi.org/10.1210/jc.2003-031414.

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Diabetes and ovarian senescence are associated with impaired endothelial function and altered arterial mechanical properties. Alterations in normal vascular structure and functioning are the primary cause of mortality and morbidity with type 2 diabetes. Similarly, after menopause, women experience an increase in the rate of cardiovascular disease. Thiazolidinediones have exhibited a number of antiatherogenic actions in populations with type 2 diabetes. The effect of thiazolidinediones in combination with hormone therapy (HT) in postmenopausal women is, however, unknown. To assess whether HT (transdermal estradiol 50 μg and micronized progesterone (100 mg/d) affects vascular function, 21 women receiving rosiglitazone were randomly assigned to receive HT or placebo for 12 wk in a double-blind crossover design. Measures of glycemic control, lipids, blood pressure, flow-mediated dilation, and distensibility index were undertaken at baseline and after each treatment. As a result, flow-mediated dilation was significantly reduced (15.3 ± 3.8 to 6.6 ± 1.6%, P = 0.02) with HT, whereas lipids, blood pressure, and distensibility index were unchanged. Placebo had no significant affect on any variables. Thus, the addition of HT to rosiglitazone treatment attenuates endothelial function without altering other cardiovascular risk factors. Caution should, therefore, be exercised when considering combined treatment with thiazolidinedione and HT.

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31

Petunina, N. A., E. V. Goncharova, I. A. Kuzina, L. V. Nedosugova, N. S. Martirosyan, and M. Е. Теlnova. "The role of pioglitazone in the fight against insulin resistance, atherosclerosis, cardiovascular disease, and non-alcoholic fatty liver disease." Diabetes mellitus 25, no. 5 (November 30, 2022): 504–13. http://dx.doi.org/10.14341/dm12859.

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Modern strategies for the treatment of type 2 diabetes mellitus involve the use of pathogenetically based approaches aimed at achieving optimal glycemic control and its long-term retention. Timely and rational use of 9 classes of hypoglycemic drugs, including as part of combination therapy, makes it possible to achieve significant success in diabetes therapy. One of the fundamental principles in the treatment of type 2 diabetes mellitus is the effect on insulin resistance. For this purpose, two groups of drugs are used: biguanides and thiazolidinediones (glitazones). The action of glitazones is directly related to an increase in the sensitivity of insulin-dependent tissues to insulin and a pronounced decrease in hyperinsulinemia in patients with type 2 diabetes. Of particular interest are the pathways of insulin signal transduction, the mechanisms of insulin resistance, and the possibilities of pathogenetic therapy with thiazolidinediones. Pioglitazone is currently the only available member of the thiazolidinedione class in the world, allowing to expand the management of diabetes mellitus by reducing insulin resistance in muscle and adipose tissue and glucose production by the liver. Its use can have a number of pleiotropic effects, including on cardiovascular diseases and non-alcoholic fatty liver disease, which expands the priorities for choosing hypoglycemic therapy in patients with type 2 diabetes at various stages of therapy.

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Hart, C. Michael. "The Role of PPARγ in Pulmonary Vascular Disease." Journal of Investigative Medicine 56, no. 2 (February 1, 2008): 518–21. http://dx.doi.org/10.2310/jim.0b013e318165e921.

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The peroxisome proliferator-activated receptor (PPAR) γ is a member of the nuclear hormone receptor superfamily of ligand-activated transcription factors. Thiazolidinediones, pharmacological ligands for PPARγ, are currently used in the management of type 2 diabetes. Peroxisome proliferator-activated receptor γ is expressed in the lung and pulmonary vasculature, and its expression is reduced in the vascular lesions of patients with pulmonary hypertension. Furthermore, thiazolidinedione PPARγ ligands reduced pulmonary hypertension and vascular remodeling in several experimental models of pulmonary hypertension. This report reviews current evidence that PPARγ may represent a novel therapeutic target in pulmonary hypertension and examines studies that have begun to elucidate mechanisms that underlie these potential therapeutic effects.

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33

Lytvynenko, N., and M. Yu Delva. "Thiazolidinediones and ischemic stroke (literature review and reasoning for the new potential treatment approaches)." NATIONAL JOURNAL OF NEUROLOGY, no. 2 (January 19, 2019): 26–34. http://dx.doi.org/10.28942/nnj.v1i2.228.

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Stroke is a leading cause of death and disability among adult population. Many pathological events including inflammation, oxidative stress, and apoptosis contribute to the secondary neuronal death after stroke. The goal of this review is to discuss the therapeutic potential and putative mechanisms of neuroprotective properties of thiazolidinediones (peroxisome proliferator-activated receptors-γ agonists) at ischemic stroke. Thiazolidinediones have insulin-sensitizing and other additional pleiotropic properties. Ischemic neuroprotection afforded by thiazolidinediones has been involved anti-inflammatory, anti-oxidant, anti-apoptotic properties, as well as effects on endothelial function and repair. These novel actions of thiazolidinediones could offer some protection against the potentially enhanced damage of brain ischemia in patients with abdominal obesity and insulin resistance and may open new exciting lines of investigation on stroke treatment.

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34

Al Bratty, Mohammed, Ayman Q. Hakami, Hatim A. Masmali, Md Shamsher Alam, Hassan A. Alhazmi, Neelaveni Thangavel, Asim Najmi, Sivakumar S. Moni, and Anzarul Haque. "The Spectrum of Thiazolidinediones against Respiratory Tract Pathogenic Bacteria: An In Vitro and In Silico Approach." Current Pharmaceutical Biotechnology 21, no. 14 (December 7, 2020): 1457–69. http://dx.doi.org/10.2174/1389201021666200618161210.

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Background and Objectives: Drug design strategies to develop novel broad-spectrum antibacterial agents for the treatment of respiratory tract infections that can combat bacterial resistance are currently gaining momentum. 2,4-thiazolidinedione is a structural scaffold that contains pharmacophores similar to β-lactam and non- β-lactam antibiotics. The objective of the study was to synthesize newer 3,5-Disubstituted-2,4-Thiazolidinediones (DTZDs) and subject them to in vitro antibacterial screening against bacterial pathogens. Also, we performed in silico docking of selected compounds to penicillin-binding proteins and beta-lactamases. Methods: Intermediate Schiff bases were prepared by the reaction between 2,4-thiazolidinedione and an appropriate aldehyde followed by acylation of the ring nitrogen with 3-brompropanoyl chloride resulting in DTZDs. Minimum inhibitory concentrations were determined against few bacteria infecting the respiratory tract by the broth tube dilution method. Zones of inhibitions against the bacteria were also determined using agar well diffusion technique. Molecular docking of the compounds to all types of Penicillin-Binding Proteins (PBPs) and β-lactamases was also carried out. Results: Compounds DTZD12 and DTZD16 exhibited broad-spectrum antibacterial activity. The minimum inhibitory concentrations of the compounds were 175μg/100μL. Measurements of the zones of inhibitions indicated that compound DTZD12 was more active than DZTD16. E. coli was the most susceptible organism. Docking results established that both the compounds were able to interact with PBPs and β-lactamases through strong hydrogen bonds, especially the unique interaction with active serine residue of the PBP for inhibition of cell wall synthesis. Conclusion: DTZD12 and DTZD16 can be developed into antibacterial drugs for respiratory tract infections to oppose bacterial resistance, or can also be used as leads for repurposing the existing 2,4- thiazolidinediones.

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35

Wong, Carlos K. H., Kenneth K. C. Man, Esther W. Y. Chan, Tingting Wu, Emily T. Y. Tse, Ian C. K. Wong, and Cindy L. K. Lam. "DPP4i, thiazolidinediones, or insulin and risks of cancer in patients with type 2 diabetes mellitus on metformin–sulfonylurea dual therapy with inadequate control." BMJ Open Diabetes Research & Care 8, no. 1 (June 2020): e001346. http://dx.doi.org/10.1136/bmjdrc-2020-001346.

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IntroductionThis study aims to compare the risks of cancer among patients with type 2 diabetes mellitus (T2DM) on metformin–sulfonylurea dual therapy intensified with dipeptidyl peptidase 4 inhibitors (DPP4i), thiazolidinediones, or insulin.Research design and methodsWe assembled a retrospective cohort data of 20 577 patients who were free of cancer and on metformin–sulfonylurea dual therapy, and whose drug treatments were intensified with DPP4i (n=9957), insulin (n=7760), or thiazolidinediones (n=2860) from January 2006 to December 2017. Propensity-score weighting was used to balance out baseline covariates across the three groups. HRs for any types of cancer, cancer mortality, and all-cause mortality were assessed using Cox proportional-hazards models.ResultsOver a mean follow-up period of 34 months with 58 539 person-years, cumulative incidences of cancer, cancer mortality, and all-cause mortality were 0.028, 0.009, and 0.072, respectively. Patients intensified with insulin had the highest incidence of all-cause mortality (incidence rate=3.22/100 person-years) and the insulin itself posed the greatest risk (HR 2.46, 95% CI 2.25 to 2.70, p<0.001; 2.44, 95% CI 2.23 to 2.67) compared with thiazolidinediones and DPP4i, respectively. Comparing between thiazolidinediones and DPP4i, thiazolidinediones was associated with higher risk of cancer (HR 1.43, 95% CI 1.25 to 1.63) but not cancer mortality (HR 1.21, 95% CI 0.92 to 1.58) and all-cause mortality (HR 0.99, 95% CI 0.88 to 1.11). Insulin was associated with the greatest risk of cancer mortality (HR 1.36, 95% CI 1.09 to 1.71; 1.65, 95% CI 1.31 to 2.07) compared with thiazolidinediones and DPP4i, respectively.ConclusionsFor patients with T2DM on metformin–sulfonylurea dual therapy, the addition of DPP4i was the third-line medication least likely to be associated with cancer mortality and cancer effect among three options, and posed no increased risk for all-cause mortality when compared with thiazolidinediones.

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Smith, Ulf. "Thiazolidinedione-induced effects beyond glycaemic control." British Journal of Diabetes & Vascular Disease 2, no. 1_suppl (January 2002): S24—S27. http://dx.doi.org/10.1177/1474651402002001s0601.

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The thiazolidinediones exert their insulin sensitising effect by binding to the nuclear receptors (transcription factors) peroxisome proliferator activated receptor (PPAR) γ and, to varying degrees, to PPARα. Several different genes are activated by thiazolidinediones, many of which contribute to the increase in insulin sensitivity (eg. an increase in glucose uptake and utilisation, a decrease in gluconeogenesis and in insulin-antagonistic cytokines, such as tumour necrosis factor α). Activation of other genes indirectly reduces insulin resistance by, for example, increasing free fatty acid (FFA) uptake and oxidation resulting in lower circulating FFA levels. The action of thiazolidinediones at PPARγ is generally responsible for their insulin sensitising effects while action at PPARα contributes to their lipid lowering effects. Therefore, the relative affinities of the different thiazolidinediones for PPARγ and PPARα will also lead to a different spectrum of actions for each agent.

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Palmer, Andrew J., William J. Valentine, and Joshua A. Ray. "Thiazolidinediones for Diabetes Mellitus." Disease Management & Health Outcomes 12, no. 6 (2004): 363–75. http://dx.doi.org/10.2165/00115677-200412060-00003.

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Grey, Andrew B. "Skeletal Toxicity of Thiazolidinediones." Annals of Internal Medicine 148, no. 7 (April 1, 2008): 563. http://dx.doi.org/10.7326/0003-4819-148-7-200804010-00020.

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Scheen, Andr?? J. "Pharmacokinetic Interactions with Thiazolidinediones." Clinical Pharmacokinetics 46, no. 1 (2007): 1–12. http://dx.doi.org/10.2165/00003088-200746010-00001.

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&NA;. "Thiazolidinediones in the spotlight." Inpharma Weekly &NA;, no. 1607 (September 2007): 4. http://dx.doi.org/10.2165/00128413-200716070-00004.

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Suwattee, Pitiporn, Cyrus DeSouza, Sunil Asnani, Lucia Gilling, and Vivian A. Fonseca. "Cardiovascular Effects of Thiazolidinediones." Endocrinologist 12, no. 2 (March 2002): 126–34. http://dx.doi.org/10.1097/00019616-200203000-00011.

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Goldberg, Ronald B. "Thiazolidinediones and vascular damage." Current Opinion in Endocrinology, Diabetes and Obesity 14, no. 2 (April 2007): 108–15. http://dx.doi.org/10.1097/med.0b013e328054c655.

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Wilson, Carol. "Thiazolidinediones increase fracture risk." Nature Reviews Endocrinology 5, no. 12 (December 2009): 641. http://dx.doi.org/10.1038/nrendo.2009.205.

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Barnett, Anthony H. "Thiazolidinediones and cardiovascular outcomes." British Journal of Diabetes & Vascular Disease 8, no. 1 (January 2008): 45–49. http://dx.doi.org/10.1177/14746514080080011001.

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Stumvoll, Michael. "Thiazolidinediones – some recent developments." Expert Opinion on Investigational Drugs 12, no. 7 (July 2003): 1179–87. http://dx.doi.org/10.1517/13543784.12.7.1179.

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Colca, J. R., W. G. McDonald, and R. F. Kletzien. "Mitochondrial target of thiazolidinediones." Diabetes, Obesity and Metabolism 16, no. 11 (May 22, 2014): 1048–54. http://dx.doi.org/10.1111/dom.12308.

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He, Lingling, Xiaoli Liu, Lijia Wang, and Zhiyun Yang. "Thiazolidinediones for nonalcoholic steatohepatitis." Medicine 95, no. 42 (October 2016): e4947. http://dx.doi.org/10.1097/md.0000000000004947.

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Rizos, CV, EN Liberopoulos, DP Mikhailidis, and MS Elisaf. "Pleiotropic effects of thiazolidinediones." Expert Opinion on Pharmacotherapy 9, no. 7 (April 21, 2008): 1087–108. http://dx.doi.org/10.1517/14656566.9.7.1087.

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Kiryluk, K., and R. Isom. "Thiazolidinediones and fluid retention." Kidney International 72, no. 6 (September 2007): 762–68. http://dx.doi.org/10.1038/sj.ki.5002442.

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Mayhew, Maren. "Thiazolidinediones—the Ongoing Debate." Journal for Nurse Practitioners 3, no. 10 (November 2007): 722–23. http://dx.doi.org/10.1016/j.nurpra.2007.09.003.

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