al . (2012) indicated that rosiglitazone-induced activation of Pparγ reduced collagen and osteocalcin (BGLAP) levels in mouse primary bone marrow-derived MSCs and prevented the mRNA expression of Runx2 . These inhibitory effects of Pparγ
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M van de Vyver, E Andrag, I L Cockburn, and W F Ferris
Bee K Tan, Krzysztof C Lewandowski, Joseph Paul O'Hare, and Harpal S Randeva
rosiglitazone increase adipolin expression in mouse adipocytes ( Wei et al . 2012 b ). However, to date, adipolin receptors have yet to be determined. Recently, we had reported that circulating and adipose tissue adipolin levels are significantly lower in women
M Alexandra Sorocéanu, Dengshun Miao, Xiu-Ying Bai, Hanyi Su, David Goltzman, and Andrew C Karaplis
Introduction Thiazolidinediones (TZDs) are a novel class of insulin-sensitizing antidiabetic agents. In the USA and Canada, two TZDs are indicated for use in type 2 diabetes mellitus, rosiglitazone and pioglitazone. A third
Victor P Bilan, Eman M Salah, Sheldon Bastacky, Huw B Jones, Rachel M Mayers, Bradley Zinker, Simon M Poucher, and Stevan P Tofovic
criteria for DN in rodents ( Brosius et al . 2009 ) and the recently published classification of DN in humans ( Tervaert et al . 2010 ). Thiazolidinediones (TZDs), including rosiglitazone, are high-affinity ligands for peroxisome proliferator
Guohong Liu, Mirta Grifman, James Macdonald, Peter Moller, Flossie Wong-Staal, and Qi-Xiang Li
-Adrenergic stimulation inhibits adiponectin gene expression, indicating a possible role of the adiponectin reduction in catecholamine-induced insulin resistance ( Fasshauer et al. 2003 ). Rosiglitazone, a PPARγ agonist, ameliorates insulin resistance at least partially
Guoyue Yuan, Xia Chen, Qinyun Ma, Jie Qiao, Rongying Li, Xuesong Li, Shengxian Li, Jinfeng Tang, Libin Zhou, Huaidong Song, and Mingdao Chen
-isobutyl-xanthine, anti-adiponectin antibody, AG490, PD98059, SB203580, and LY294002 were purchased from Sigma. Human recombinant CRP was obtained from Calbiochem (La Jolla, CA, USA). Rosiglitazone was generously provided by Shanghai Sunve Pharmaceutical Co., Ltd. Goat
Harn-Shen Chen, Tzu-En Wu, Chi-Chang Juan, and Hong-Da Lin
myocardial HSPD1, the study used rosiglitazone and amlodipine to treat fructose-fed rats. Rosiglitazone is an agonist for peroxisome proliferator-activated receptor γ, which is a ligand-activated nuclear transcription factor that lowers blood glucose
Sujith Rajan, Ganesh Panzade, Ankita Srivastava, Kripa Shankar, Rajesh Pandey, Durgesh Kumar, Sanchita Gupta, Abhishek Gupta, Salil Varshney, Muheeb Beg, Raj Kumar Mishra, Ravi Shankar, and Anil Gaikwad
capacity compared to CI-induced IR adipocytes transduced with Lenti-Con inhibitor ( Fig. 7C ). Thiazolidinedione classes of compounds such as rosiglitazone are known for their anti-diabetic effect and are prescribed for IR treatment ( Chiarelli & Di Marzio
AG Gunin, AD Bitter, AB Demakov, EN Vasilieva, and NV Suslonova
It is suggested that the action of peroxisome proliferator-activated receptors (PPARs) cross-talks with estrogen signaling in the uterus. However, it is not known how PPAR agonists affect estrogen-dependent processes in the uterus, especially proliferation and morphogenetic changes. The effects of agonists of PPAR-alpha and -gamma on proliferative and morphogenetic reactions in the uterus under short- and long-term estrogen treatments were therefore examined. Ovariectomized mice were treated with estradiol dipropionate (4 micro g/100 g, s.c., once a week) or vehicle and rosiglitazone (PPAR-gamma agonist) or fenofibrate (PPAR-alpha agonist) or with no additional treatment for 2 days or for 30 days. Treatment with estradiol and PPAR agonists for 2 days did not affect uterine mass. In mice treated with estradiol and rosiglitazone for 2 days, proliferation was enhanced and levels of estrogen receptors-alpha and beta-catenin were decreased in all uterine tissues. Treatment with estradiol and fenofibrate for 2 days had the opposite effects on the parameters tested. In animals treated with estradiol and rosiglitazone for 30 days, uterine mass was increased, abnormal uterine glands and atypical endometrial hyperplasia were found more often and levels of estrogen receptors-alpha and beta-catenin were decreased. In animals treated with estradiol and fenofibrate for 30 days, uterine mass was decreased, most of the uterine glands had a normal structure, no cases of atypical hyperplasia were diagnosed, proliferative activity was declined and the levels of estrogen receptors-alpha and beta-catenin were markedly higher. Treatment with rosiglitazone or fenofibrate did not affect the serum estradiol level in the mice which received estradiol together with PPAR agonists for 30 days. Thus, rosiglitazone exerted the proliferative and morphogenetic effects of estradiol, but fenofibrate had the opposite effect. The actions of rosiglitazone and fenofibrate are associated with changes in the expression of estrogen receptors-alpha and beta-catenin in the uterus.
C Crescioli, L Cosmi, E Borgogni, V Santarlasci, S Gelmini, M Sottili, E Sarchielli, B Mazzinghi, M Francalanci, A Pezzatini, G Perigli, G B Vannelli, F Annunziato, and M Serio
comparison a peroxisome proliferator-activated receptor γ (PPARγ) agonist, rosiglitazone (RGZ), a drug for type 2 diabetes treatment, since it has been recently reported to suppress IFNγ+TNFα-induced CXCL10 secretion in human thyroid follicular cells of GD
