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Relevant bibliographies by topics / Rosiglitazone

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Academic literature on the topic 'Rosiglitazone'

Author: Grafiati

Published: 4 June 2021

Last updated: 10 March 2023

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Journal articles on the topic "Rosiglitazone"

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Okami, Nobuya, Purnima Narasimhan, Hideyuki Yoshioka, Hiroyuki Sakata, Gab Seok Kim, Joo Eun Jung, Carolina M. Maier, and Pak H. Chan. "Prevention of JNK Phosphorylation as a Mechanism for Rosiglitazone in Neuroprotection after Transient Cerebral Ischemia: Activation of Dual Specificity Phosphatase." Journal of Cerebral Blood Flow & Metabolism 33, no. 1 (October 3, 2012): 106–14. http://dx.doi.org/10.1038/jcbfm.2012.138.

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Rosiglitazone, a synthetic peroxisome proliferator-activated receptor-γ (PPARγ) agonist, prevents cell death after cerebral ischemia in animal models, but the underlying mechanism has not been clarified. In this study, we examined how rosiglitazone protects neurons against ischemia. Mice treated with rosiglitazone were subjected to 60 minutes of focal ischemia followed by reperfusion. Rosiglitazone reduced infarct volume after ischemia and reperfusion. We show that this neuroprotective effect was reversed with a PPARgM antagonist. Western blot analysis showed a significant increase in expression of phosphorylated stress-activated protein kinases (c-Jun N-terminal kinase (JNK) and p38) in ischemic brain tissue. Rosiglitazone blocked this increase. Furthermore, we observed that rosiglitazone increased expression of the dual-specificity phosphatase 8 (DUSP8) protein and messenger RNA in ischemic brain tissue. Dual-specificity phosphatase 8 is a mitogen-activated protein kinase phosphatase that can dephosphorylate JNK and p38. Another key finding of the present study was that knockdown of DUSP8 in primary cultured cortical neurons that were subjected to oxygen–glucose deprivation diminished rosiglitazone's effect on downregulation of JNK phosphorylation. Thus, rosiglitazone's neuroprotective effect after ischemia is mediated by blocking JNK phosphorylation induced by ischemia via DUSP8 upregulation.

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&NA;. "Rosiglitazone." Reactions Weekly &NA;, no. 1180 (December 2007): 34. http://dx.doi.org/10.2165/00128415-200711800-00107.

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&NA;. "Rosiglitazone." Reactions Weekly &NA;, no. 1186 (January 2008): 33. http://dx.doi.org/10.2165/00128415-200811860-00106.

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&NA;. "Rosiglitazone." Reactions Weekly &NA;, no. 1127 (November 2006): 21. http://dx.doi.org/10.2165/00128415-200611270-00070.

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&NA;. "Rosiglitazone." Reactions Weekly &NA;, no. 1143 (March 2007): 21. http://dx.doi.org/10.2165/00128415-200711430-00070.

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&NA;. "Rosiglitazone." Reactions Weekly &NA;, no. 788 (February 2000): 9–10. http://dx.doi.org/10.2165/00128415-200007880-00030.

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&NA;. "Rosiglitazone." Reactions Weekly &NA;, no. 788 (February 2000): 10. http://dx.doi.org/10.2165/00128415-200007880-00031.

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&NA;. "Rosiglitazone." Reactions Weekly &NA;, no. 850 (May 2001): 11. http://dx.doi.org/10.2165/00128415-200108500-00028.

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&NA;. "Rosiglitazone." Reactions Weekly &NA;, no. 1400 (May 2012): 37. http://dx.doi.org/10.2165/00128415-201214000-00137.

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&NA;. "Rosiglitazone." Reactions Weekly &NA;, no. 1199 (April 2008): 40–41. http://dx.doi.org/10.2165/00128415-200811990-00123.

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Dissertations / Theses on the topic "Rosiglitazone"

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Pereira, Lúciano Artur Lopes. "Characterization of the sympathomimetic action of rosiglitazone." Master's thesis, Faculdade de Medicina da Universidade do Porto, 2009. http://hdl.handle.net/10216/53524.

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Pereira, Lúciano Artur Lopes. "Characterization of the sympathomimetic action of rosiglitazone." Dissertação, Faculdade de Medicina da Universidade do Porto, 2009. http://hdl.handle.net/10216/53524.

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Matos, Amélio Fernando de Godoy. "Relação entre a Síndrome Metabólica, teor de gordura intramiocelular e os níveis plasmáticos da Adiponectina: papel da Rosiglitazona." Universidade do Estado do Rio de Janeiro, 2009. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=1421.

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A resistência à insulina está associada com o aumento do teor de gordura intramiocelular (GIMC) e com níveis séricos da adiponectina (ADP) diminuídos. A ADP por sua vez está envolvida na oxidação de gordura muscular. Entretanto, a relação entre ambas continua controversa. O objetivo deste estudo é explorar a relação entre a ADP e a GIMC em adultos não diabéticos, além de estudar o papel da rosiglitasona (RSG) sobre a distribuição da gordura entre os compartimentos musculares. Este estudo compreende duas fases: uma fase transversal (corte-transversal) e uma fase longitudinal, de intervenção terapêutica com uma droga, num desenho aberto. Laboratório de Pesquisas Clínicas e Experimentais em Biologia Vascular (Biovasc) - UERJ. Material e métodos Na fase transversal, 24 pacientes obesos, não diabéticos, com síndrome metabólica (SM) e 9 controles magros e saudáveis foram estudados. Foi realizada a Espectroscopia de Prótons por Ressonância Nuclear Magnética (1H-ERNM) para quantificar a gordura extramiocelular (GEMC) e a GIMC. Estas, associadas à ADP e aos parâmetros antropométricos e bioquímicos, foram avaliadas e comparadas nos dois grupos. Durante a fase longitudinal, 15 destes pacientes foram reestudados, através da 1H-ERNM, após o tratamento com RSG por 6 meses. Da mesma forma, as variáveis antropométricas e metabólicas foram reavaliadas. Fase transversal: os pacientes com SM apresentaram maior índice de massa corporal (IMC), cintura abdominal, relação cintura-quadril (RCQ), e níveis de glicemia, insulina e triglicerídeos e menores níveis de HDL-c, quando comparados com o grupo controle. Da mesma forma o HOMA-RI [3.25 (2.58-4.13) vs 1.02 (0.73-1.29); p<0.0001] e a GIMC [266.1 (189.9-296.3) vs 72.85 (55.3-109.4) unidades arbitrárias-UA, p<0.0001] estavam aumentados enquanto o QUICKI [0.32 (0.31-0.33) vs 0.38 (0.37-0.40); p<0.0001] e a ADP [8.6 (4.05-15.95) vs 21.1 (12.9-24.4) μg/ml; p=0.02) estavam diminuídos. O teor de GIMC associou-se diretamente com a glicose, insulina, triglicerídeos e HOMA-RI e inversamente com o HDL-c, QUICKI e, mais importantemente, com a ADP (r = -0.41; p<0.05). Fase longitudinal: após o tratamento com RSG, o peso corporal e a circunferência do quadril aumentaram, respectivamente [100.9 (91.12-138.7) vs 107,0 (79.6-142.8) kg e 118 (107-126) cm vs 122 (110-131) cm]; enquanto a RCQ diminuiu [0.93 (0.87-1.00) vs 0.89 (0.82-0.97); P<0.001 para todos]. Adicionalmente, a glicemia, a insulina e o HOMA-RI diminuíram significativamente, enquanto a ADP aumentou mais de 3 vezes [9.7 (3.7-17.7) vs 38.0 (19.3-42.4) μg/ml]. Finalmente, a GIMC não se modificou [267.54 (213.94-297.94) vs 305.75 (230.80-424.75) UA], mas a GEMC aumentou de forma significativa [275.53 (210.39-436.66) vs 411.39 (279.92-556.59) UA; P<0.01] diminuindo a razão GIMC sobre GEMC [GIMC/GEMC; 1.07 (0.78-1.23) vs. 0.71 (0.53-0.96); p<0.01]. A ADP correlacionou-se inversamente com o teor da GIMC em adultos obesos não diabéticos com SM. Este achado tem possíveis implicações para o papel da ADP na oxidação da gordura muscular, na RI e na SM. O tratamento com RSG aumentou a massa corporal e a circunferência do quadril e diminuiu a RCQ. Além disso, diminuiu a razão GIMC/GEMC, por aumentar a GEMC sem alterar significativamente a GIMC. Isto sugere que este medicamento pode prevenir a deposição da gordura no compartimento intramiocelular ao aumentar os depósitos periféricos e o extramiocelular.
Insulin resistance (IR) is associated with intramyocellular lipid (IMCL) content and low serum adiponectin (ADP) levels. ADP is also involved in muscle fat oxidation but the relationship between them is still controversial. We aimed to further explore the relationship between ADP and IMCL content in non-diabetic adults and the role of rosiglitazone (RSG) in muscle fat compartment distribution in an adult population of obese nondiabetic metabolic syndrome patients. This study comprises two phases: a cross-sectional and a longitudinal, open-label, drug-interventional one. Laboratory for Clinical and Experimental Research on Vascular Biology (Biovasc) at the State University of Rio de Janeiro. During the cross-sectional phase, 24 obese, nondiabetic patients with metabolic syndrome (MS) and 9 lean healthy controls were studied. Proton nuclear magnetic resonance spectroscopy (1H-NMRS) was performed to quantify IMCL, as well as extramyocellular lipid (EMCL) content. The latter plus serum ADP, anthropometrics and biochemical parameters were evaluated and compared in these two groups. During the longitudinal phase, fifteen of the MS patients were studied by means of 1HNMRS before and after treatment with 8mg/day of RSG for 6 months. Anthropometrical and metabolic variables were assessed. Measurements and main results cross-sectional phase: MS patients had higher body mass index (BMI), waist, waist-to-hip ratio (WHR), glucose, insulin and triglycerides and lower HDL-c as compared to controls. HOMA-IR (3.25 [2.58-4.13] vs 1.02 [0.73-1.29]; p<0.0001) and IMCL content (266.1 [189.9-296.3] vs 72.85 [55.3-109.4) AU, p<0.0001] were higher, and QUICKI (0.32 [0.31-0.33] vs 0.38 [0.37-0.40]; p<0.0001) and ADP (8.6 [4.05-15.95] vs 21.1 [12.9-24.4] μg/ml; p=0.02) lower in MS compared to controls. IMCL content was directly associated with glucose, insulin, triglycerides and HOMAxiii IR and inversely to HDLc, QUICKI and, more importantly, with ADP (r = -0.41; p<0.05). Longitudinal phase: After RSG treatment, body weight and hip circumference increased [100.9 (91.12-138.7) vs 107,0 (79.6-142.8) kg and 118 (107-126) cm vs 122 (110-131) cm] respectively, while WHR decreased [0.93 (0.87-1.00) vs 0.89 (0.82-0.97); P<0.001 for all]. Additionally, fasting plasma glucose, insulin and HOMA-IR significantly decreased while adiponectin increased over 3 fold [9.7 (3.7-17.7) vs 38.0 (19.3-42.4) μg/ml]. Finally, IMCL did not change [267.54 (213.94-297.94) vs 305.75 (230.80-424.75) arbitrary units (AU)] while EMCL increased [275.53 (210.39-436.66) vs 411.39 (279.92-556.59) AU; P<0.01] therefore decreasing IMCL to EMCL ratio (IMCL/EMCL) [1.07 (0.78-1.23) vs. 0.71 (0.53-0.96); p<0.01]. ADP is inversely related to IMCL content in non-diabetic adults. This finding has possible implications for the role of ADP in muscle fat oxidation, IR and MS. RSG treatment increased body weight and hip circumference decreasing WHR and decreased IMCL/EMCL ratio by increasing EMCL without any significant change on IMCL, thus suggesting that this drug may prevent IMCL fat deposition by increasing EMCL and peripheral deposits.

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McClure, Lauren Elizabeth. "Best of Both Worlds: Linking Nitric Oxide Donors and Rosiglitazone." Thesis, The University of Arizona, 2014. http://hdl.handle.net/10150/321882.

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Ali, Tomader Faroug Mohammed. "Protection of pancreatic beta cells by Rosiglitazone : mechanisms and pathways." Thesis, University of Brighton, 2011. https://research.brighton.ac.uk/en/studentTheses/a2865a73-c579-4bf0-a80f-2b609425cc17.

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The thiazolidinedione Rosiglitazone can protect pancreatic beta cells from the detrimental effects of free fatty acids. The aim of this study was to determine the differential effects of saturated fatty acids on beta cells and to identify the mechanisms through which Rosiglitazone can protect beta cell viability. Utilising the mouse beta cell line MIN6, transmission electron microscopy (TEM) was used to determine the effects of palmitate and Rosiglitazone on lipid uptake and cell ultra-structure. H/PI staining and MTT assays were used to determine cell viability.

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Sidhu, Jagdip Singh. "The effects of rosiglitazone, a peroxisome proliferator-activated receptor ÃŽÂ³ ligand, on atherosclerosis." Thesis, St George's, University of London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407397.

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Ferreira, Iolanda João Mora Cruz de Freitas. "Pre and postjunctional effects of rosiglitazone on the isolated rat aorta and heart." Master's thesis, Faculdade de Medicina da Universidade do Porto, 2010. http://hdl.handle.net/10216/61097.

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Ferreira, Iolanda João Mora Cruz de Freitas. "Pre and postjunctional effects of rosiglitazone on the isolated rat aorta and heart." Dissertação, Faculdade de Medicina da Universidade do Porto, 2010. http://hdl.handle.net/10216/61097.

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Dias, Cristiano. "Rosiglitazone pode causar lesão tubular renal em ratos normais mas não em ratos hipercolesterolêmicos." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-25022010-160938/.

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Introdução: Rosiglitazone (RGL) é um ligante dos receptores PPAR e vem sendo usada no tratamento do Diabetes Mellitus tipo 2 e nas doenças inflamatórias. Mas, RGL pode reduzir a filtração glomerular (FG), a carga excretada de sódio na urina (UVNa) e aumentar a expressão da Na+,K+- ATPase na medula renal. Então, RGL pode causar edema e insuficiência cardíaca congestiva. Entretanto, não tem sido reportado se RGL pode induzir insuficiência renal aguda (IRA). Objetivo: Verificar se a redução da FG causada pelo tratamento com RGL predispõe à IRA em ratos. Avaliar em condições basais e de vasoconstrição renal e se há diferenças entre ratos normocolesterolêmicos (NC) e hipercolesterolêmicos (HC). Métodos: A FG foi medida pelo clearance de inulina no 8º dia em ratos (~200g) NC e HC tratados ou não com RGL (48 mg/kg/dieta) na situação basal e durante a infusão endovenosa de Ang II (40 ng/kg/min). Além disso, a atividade da Na+,K+-ATPase foi avaliada em homogenato renal em outra série de animais. Resultados: Na situação basal, NC e HC apresentaram FG semelhante e o tratamento com RGL reduziu a FG apenas em NC de 0,78±0,03 para 0,50±0,05* ml/min/100g, *p<0,001. Apesar da redução da FG, a UVNa em NC+RGL não se modificou. Durante a infusão de Ang II, a FG de NC, HC e HC+RGL reduziu-se para o mesmo patamar de NC+RGL e um significante aumento da UVNa foi observada apenas em NC+RGL (NC= 3,32±0,88; NC+RGL=5,86±1,04*; HC= 2,63±0,43 e HC+RGL= 2,23±0,39 uEq/min, *p<0,01). Além disso, RGL induziu aumento na atividade da Na+,K+-ATPase em HC+RGL e não modificou em NC+RGL. Os valores expressos em M Pi/mg proteína.h-1 foram de 45±7 em NC, 43±5 em NC+RGL, 48±7 em HC e 64±4* em HC+RGL, *p<0,05. Analisando todos os resultados em conjunto, a redução da FG associada com a alta natriurese e ausência da modulação da atividade da Na+,K+-ATPase em NC+RGL sugerem lesão renal neste grupo. Conclusão: Os mecanismos de ação da RGL diferem de acordo com a condição metabólica. Então, RGL deve ser prescrita com cautela na ausência de hipercolesterolemia e requer a monitoração da função renal principalmente nas situações de vasoconstrição
Introduction: Rosiglitazone (RGL) is a ligand for PPAR used to treat type 2 Diabetes Mellitus and inflammatory diseases. However, RGL can reduce the glomerular filtration rate (GFR), urinary sodium excretion (UVNa) and increase the expression of Na+, K+-ATPase in renal medulla. Thus, RGL may induce edema and congestive heart failure. However, acute renal failure (ARF) provoked by RGL treatment has not been reported. Aim: To test whether reduced GFR by RGL may predispose to ARF at baseline and during a renal vasoconstriction state, and if the findings differ between normocholesterolemic (NC) and hypercholesterolemic (HC) rats. Methods: GFR was measured by inulin clearance on the 8th day in NC and HC rats (~200g) treated or not with RGL (48 mg/kg diet) at baseline and during intravenous infusion of Ang II (40 ng/kg/min). Furthermore, the Na+,K+- ATPase activity was determined in renal homogenates in other series of animals. Results: At baseline, NC and HC had similar GFR and the treatment with RGL reduced GFR only in NC from 0.78±0.03 to 0.50±0.05* ml/min/100g, *p<0.001. Although GFR was reduced, UVNa was unchanged in NC+RGL. During Ang II infusion, GFR was significantly reduced in NC, HC and HC+RGL and it remained at the same reduced level in NC+RGL. At this time, when GFR was reduced the same range in all groups, a significant increment in UVNa was only observed in NC+RGL (NC = 3.32±0.88; NC+RGL = 5.86±1.04*; HC = 2.63±0.43 and HC+RGL = 2.23±0.39 Eq/min, *p<0.01). Moreover, RGL induced an increase in the activity of Na+, K+-ATPase in HC+RGL, but it did not modify the activity of this enzyme in NC+RGL. The values expressed in M Pi/mg.protein.h-1 were 45±7 in NC, 43±5 in NC+RGL, 48±7 in HC and 64±4* in HC+RGL, *p<0.05. Taken together, reduction in GFR associated with high natriuresis and without changes in the Na+, K+-ATPase activity in renal medulla of NC+RGL may suggest renal injury in this group. Conclusion: RGL may act distinctly in normocholesterolemia and in hypercholesterolemia. Thus, RGL may be prescribed with caution in absence of hypercholesterolemia and requires monitoring of renal function specially if a renal vasoconstriction state is associated.

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Woods, Sally. "Comparison of metformin, rosiglitazone, and acetaminophen in the prevention of olanzapine toxicity in mice." University of Cincinnati / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1305892985.

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Books on the topic "Rosiglitazone"

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Parker, Philip M., and James N. Parker. Rosiglitazone: A medical dictionary, bibliography, and annotated research guide to Internet references. San Diego, CA: ICON Health Publications, 2004.

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Canadian Coordinating Office for Health Technology Assessment., ed. Comparative clinical and budget evaluations of rosiglitazone and pioglitazone with other anti-diabetic agents. Ottawa: Canadian Coordinating Office for Health Technology Assessment, 2003.

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Pharm, Boucher Michel B., and Canadian Coordinating Office for Health Technology Assessment., eds. Efficacy of rosiglitazone and pioglitazone compared to other anti-diabetic agents: Systematic review and budget impact analysis. Ottawa: Canadian Coordinating Office for Health Technology Assessment, 2002.

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Pharm, Boucher Michel B., and Canadian Coordinating Office for Health Technology Assessment., eds. Efficacy of rosiglitazone and pioglitazone compared to other anti-diabetic agents: Systematic review and budget impact analysis. Ottawa: Canadian Coordinating Office for Health Technology Assessment, 2002.

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FDA's role in the evaluation of Avandia's safety: Hearing before the Committee on Oversight and Government Reform, House of Representatives, One Hundred Tenth Congress, first session, June 6, 2007. Washington: U.S. G.P.O., 2008.

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Kayla, Carl. Avandia Rosiglitazone. Independently Published, 2018.

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HOPPE, Joyce. Avandia Rosiglitazone. Independently Published, 2018.

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Blokdijk, G. J. Rosiglitazone Maleate; Complete Self-Assessment Guide. CreateSpace Independent Publishing Platform, 2018.

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Rosiglitazone - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.

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Duplisea, J. Kevin. A pilot study to describe the efficacy of metformin versus rosiglitazone in HIV patients receiving protease inhibitors. 2003, 2003.

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Book chapters on the topic "Rosiglitazone"

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Uçmak, Gülin, and Burcu Esen Akkaş. "Rosiglitazone Effect on Radioiodine Uptake in a Case of Dedifferentiated Thyroid Carcinoma." In Thyroid and Parathyroid Diseases, 297–303. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78476-2_47.

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Meisner, F., A. Noack, A. Cihlar, H. Schelzig, K. H. Orend, X. Kapfer, N. Marx, and L. Sunder-Plassmann. "Rosiglitazon stabilisiert atherosklerotische Plaques." In Chirurgisches Forum 2006, 453–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/3-540-34668-6_153.

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Day, Caroline, and Clifford J. Bailey. "Rosiglitazone." In xPharm: The Comprehensive Pharmacology Reference, 1–4. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.62558-9.

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Day, C., and C. J. Bailey. "Rosiglitazone☆." In Reference Module in Biomedical Sciences. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-801238-3.97237-4.

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"Rosiglitazone." In Hale’s Medications & Mothers’ Milk™ 2019. New York, NY: Springer Publishing Company, 2018. http://dx.doi.org/10.1891/9780826150356.0913.

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"Rosiglitazone (r)." In Drugs Handbook 2012–2013. Bloomsbury Academic, 2011. http://dx.doi.org/10.5040/9781350363595.art-1531.

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Patti, Mary-Elizabeth, Mark Callery, Robert Najarian, Mandeep Sawhney, Lyle Mitzner, Alison Goldfine, and James Moser. "Case 93: Progressive Hypoglycemia Due to Insulinoma in a Patient with Type 2 Diabetes: Treatment with Image-Guided Minimally Invasive Pancreas-Sparing Surgery." In Diabetes Case Studies: Real Problems, Practical Solutions, 345–50. American Diabetes Association, 2015. http://dx.doi.org/10.2337/9781580405713.93.

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A 54-year-old man with type 2 diabetes (T2D) presented for evaluation of hypoglycemia. T2D was diagnosed at age 35 years, when the patient presented with recurrent urinary tract infections. Treatment with diet, metformin, and pioglitazone/rosiglitazone led to normalization of glucose, with hemoglobin A1c of 6%. He remained stable until age 54 years, when he developed an inferior wall myocardial infarction (MI). Postinfarction pericarditis required initiation of higher dose aspirin (650 mg t.i.d.). Patient markedly improved diet and increased exercise in the post-MI setting, achieving a rapid 24-lb weight loss. Metformin and rosiglitazone were discontinued.

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Talwalkar, Pradeep. "The Roller-Coaster Ride of Rosiglitazone—Rise, Fall and Rebirth." In Practical Diabetes Mellitus, 127. Jaypee Brothers Medical Publishers (P) Ltd., 2015. http://dx.doi.org/10.5005/jp/books/12593_15.

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G. Mallikarjuna, Beekanahalli, and Uma V. Manjappara. "Effect of GW9662 and T0070907 Antagonist of PPARg and Their Coadministration Pairwise with Obestatin on Lipid Profile of DIO-C57BL/6 Mice." In The Metabolic Role of Peroxisome in Health and Disease. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.103700.

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Obestatin and its fragment analog Nt8U were shown to upregulate glycerolipid metabolism and PPARg signaling and decrease fat accumulation in Swiss albino mice. It was further investigated if these peptides could decrease lipid accumulation under obese conditions. We chose to work on Diet-Induced-Obese (DIO) C57BL/6 mice to study the same. Both obestatin and Nt8U decreased lipid accumulation in DIO-C57BL/6 mice. PPARg was not upregulated in comparison to 60% high-fat diet (HFD) fed control mice, implying there was already enhanced PPARg expression due to HFD consumption. We also wanted to investigate if upregulation of PPARg signaling was a secondary effect of enhanced glycerolipid metabolism. To investigate the same, we administered obestatin pairwise with 2 agonists and 2 antagonists of PPARg. The results revealed obestatin is not a mere agonist of PPARg but can also decrease lipid accumulation brought about by rosiglitazone, a well-studied agonist of PPARg. The antagonists also show a further decrease in lipid accumulation, probably due to inhibition of PPARg activity brought about by HFD and the additive decrease brought about by obestatin in DIO-C57BL/6 mice. This chapter will be structured to briefly introduce obestatin, Nt8U, their effect on gene expression in the adipose tissue, and the effect of PPARg agonists and antagonists on their ability to reduce fat accumulation.

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"Behandlung mit Insulinsensitizern vom Glitazontyp (Pio-, Rosiglitazon)." In Diabetologie in Klinik und Praxis, edited by Hellmut Mehnert, Eberhard Standl, Klaus-Henning Usadel, and Hans-Ulrich Häring. Stuttgart: Georg Thieme Verlag, 2003. http://dx.doi.org/10.1055/b-0034-54553.

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Conference papers on the topic "Rosiglitazone"

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Cugno, Chiara, Ganesh Halade, and Md Mizanur Rahman. "Omega-3 fatty acid-rich fish oil supplementation prevents rosiglitazone-induced osteopenia in aging mice." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0099.

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Abstract:

Rosiglitazone is an effective insulin-sensitizer, however, associated with bone loss mainly due to increased bone resorption, and bone marrow adiposity, and decreased bone formation. We investigated the effect of the co-administration of fish oil (FO) rich in omega-3 fatty acids (FAs) on rosiglitazone (RSG)-induced bone loss in aging C57BL/6 mice and the mechanisms underlying potential preventive effect. Mice fed the iso-caloric diet supplemented with fish oil exhibited significantly higher levels of bone density in different regions compared to the other groups. In the same cohort of mice, reduced activity of COX-2, enhanced activity of alkaline phosphatase, lower levels of cathepsin k, PPAR-γ, and pro-inflammatory cytokines, and a higher level of anti-inflammatory cytokines were observed. Moreover, fish oil restored rosiglitazone-induced down-regulation of osteoblast differentiation and up-regulation of adipocyte differentiation in C3H10T1/2 cells and inhibited the up-regulation of osteoclast differentiation of RANKL-treated RAW264.7 cells. We finally tested our hypothesis on human Mesenchymal Stromal Cells (MSCs) differentiated to osteocytes and adipocytes confirming the beneficial effect of docosahexaenoic acid (DHA) omega-3 FA during treatment with rosiglitazone, through the down-regulation of adipogenic genes, such as adipsin and FABP4 along the PPARg/FABP4 axis, and reducing the capability of osteocytes to switch toward adipogenesis. Our findings demonstrate that fish oil may prevent rosiglitazone-induced bone loss by inhibiting inflammation, osteoclastogenesis, and adipogenesis and by enhancing osteogenesis in the bone microenvironment. Further clinical studies will be undertaken to establish this treatment regimen for the successful treatment of diabetic patients with rosiglitazone without adverse side effects on bone.

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Song, Eun-Kee, Ho-Young Yhim, Jun-Mo Yim, Joo-Yun Yim, Min-Young Song, Na-Ri Lee, Jae-Yong Kwak, Chang-Yeol Yim, and Myung-Hee Sohn. "Abstract 4413: Rosiglitazone prevents graft-versus-host disease (GVHD)." 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.am2012-4413.

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Benkő, Klára, Éva Pintye, Boglárka Szabó, Krisztina Géresi, Attila Megyeri, Ilona Benkő, Károly Tokési, and Béla Sulik. "Effect of Rosiglitazone on Radiation Damage in Bone Marrow Hemopoiesis." In RADIATION DAMAGE IN BIOMOLECULAR SYSTEMS: Proceedings of the 5th International Conference (RADAM 2008). AIP, 2008. http://dx.doi.org/10.1063/1.3058979.

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Ward, JE, J. Tran, SR Foster, SG Royce, ML Tang, and SR Bailey. "Bronchodilator Actions of Rosiglitazone in Isolated Mouse Trachea Are PPARγ-Independent." 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.a2432.

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Silva, AG, DM Laks, CB Magalhaes, AP Davel, LV Rossoni, CM Takiya, DS Faffe, and WA Zin. "Pulmonary Effects of Rosiglitazone in Rats Treated with Isoproterenol for One Week." 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.a6070.

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Bourke, Jane E., James Esposito, Yan Bai, and Mike Sanderson. "Rosiglitazone Inhibits Small Airway Contraction And Calcium Signalling In Mouse Lung Slices." 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.a1262.

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Tabuso, Maria, Raghu Adya, Mark Christian, and Ramesh P. Arasaradnam. "PWE-056 Rosiglitazone: a potential new stroma targeted therapeutic agent in colon cancer." In British Society of Gastroenterology Annual Meeting, 17–20 June 2019, Abstracts. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2019. http://dx.doi.org/10.1136/gutjnl-2019-bsgabstracts.380.

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Sakurai, R., E. Shin, J. Corral, J. Torday, and V. Rehan. "Antenatal Administration of PPARγ Agonist Rosiglitazone (RGZ) Prevents Hyperoxia-Induced Lung Injury Postnatally." 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.a2643.

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Oberlick, Elaine, LaTonia D. Taliaferro-Smith, Wayne Harris, Brandi B. Knight, Arumugam Nagalingam, Edmund Waller, and Dipali Sharma. "Abstract 1078: Rosiglitazone inhibits breast cancer growth and proliferation via cyclin D1 inhibition." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1078.

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Ibrahim, Khadega, Chiara Cugno, and Md Mizanur Rahman. "Conjugated Linoleic Acid (CLA) co-treatment alleviates antidiabetic drug, rosiglitazone associated deterioration of bone remodeling." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0148.

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Abstract:

Diabetes mellitus (DM) is a chronic metabolic disease characterized by hyperglycemia due to decreased insulin secretion, defective action or both. The rosiglitazone (RSG) is one of the oral antidiabetic drug used in type 2 (T2) DM and has a unique insulin-sensitizing capacity. However, RSG has a negative side effect on the bone as it stimulates the differentiation of bone marrow-mesenchymal stromal cells (BM-MSCs) into adipocytes at the expense of osteoblasts in the bone marrow microenvironment, disturbing the normal balance of bone remodeling and causing BM adiposity. On the other hand, the trans-10,cis-12 conjugated linoleic acid (CLA), a fatty acid is known as anti-adipogenic, pro-osteogenic. Therefor, this study was designed to assess whether CLA can alleviate the negative effect of RSG on bone. We used adipose tissue derived-mesenchymal stem cells (AT-MSCs) as a human in vitro model to study the effect of CLA, RSG and combined treatment (RSG+CLA) on the osteoblastogenic and adipogenic differentiation of AT-MSCs. Osteoblastogenesis was assessed by Alizarin Red Staining and bone mineralization was assessed by 〖"OsteoImage" 〗^TMassays, whereas adipogenesis was assessed by Oil Red O Staining and LipidTOX assays. Besides, the level of expression of osteogenic and adipogenic markers was measured on treated osteo- and adipo-differentiated MSCs using real time RT-PCR, immunohistochemistry (IHC) and western blot analysis. Compared to RSG group, the combined treatment group stimulates osteoblastogenesis, as evidenced by increased mineralization and upregulation of osteogenic markers OPN and RUNX2 and inhibits adipogenesis in osteogenic media as showed by decreased lipid content and downregulation of adipogenic markers FABP4, LPL and adipsin. In conclusion, the use of CLA as an adjunctive treatment reversed the effects of RSG on osteogenesis and adipogenesis. Further preclinical and clinical studies will be undertaken to establish this treatment regimen for the successful treatment of diabetic patients with rosiglitazone without adverse side effects on bone.

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