PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28481288-4 2017 Results showed that a combination of CL316,243 and rosiglitazone significantly upregulated the expression of the core thermogenic gene Ucp1 as well as genes related with mitochondrial function (Cidea, Cox5b, Cox7a1, Cox8b, and Cycs), compared with the treatment of CL316,243 or rosiglitazone alone. Rosiglitazone 51-64 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 135-139 32248079-8 2020 Combined treatment with rosiglitazone and FGF21 resulted in a synergistic increase in Ucp1 mRNA levels both in vitro and in vivo. Rosiglitazone 24-37 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 86-90 31317231-7 2019 Moreover, the administration of rosiglitazone, SIS3 and the selective beta3 adrenergic receptor agonist CL316,243 to DIO mice reduced the amount of body-fat deposits (body weight from day 0 to 14, 12.3% reduction), concomitant with morphological changes in white adipose tissue, an increase in mitochondrial biosynthesis and a marked induction of uncoupling protein 1 (UCP1). Rosiglitazone 32-45 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 347-367 31317231-7 2019 Moreover, the administration of rosiglitazone, SIS3 and the selective beta3 adrenergic receptor agonist CL316,243 to DIO mice reduced the amount of body-fat deposits (body weight from day 0 to 14, 12.3% reduction), concomitant with morphological changes in white adipose tissue, an increase in mitochondrial biosynthesis and a marked induction of uncoupling protein 1 (UCP1). Rosiglitazone 32-45 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 369-373 29910772-5 2018 Adipocytes from inguinal WAT display maximal UCP1 expression and mitochondrial uncoupling only when treated with a combination of the PPARgamma activator rosiglitazone and a beta3-adrenoceptor agonist. Rosiglitazone 154-167 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 45-49 28970184-5 2018 Treatment of brown adipocytes with rosiglitazone increases uncoupling protein 1 (UCP1) levels, and increases beta3-adrenoceptor mitochondrial function but does not affect glucose uptake responses. Rosiglitazone 35-48 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 81-85 28970184-6 2018 In contrast, inguinal white adipocytes only express UCP1 and beta3-adrenoceptors following rosiglitazone treatment, which results in an increase in all beta3-adrenoceptor-mediated functions. Rosiglitazone 91-104 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 52-56 11587528-3 2001 In this study we show that changes in MTE-1 mRNA levels as a result of differences between db/db vs db/+ mice or following long-term treatment of db/db mice with rosiglitazone or Wy-14,643 were more closely correlated with changes in UCP-3 than either UCP-1 or UCP-2 mRNA levels in the tissues examined. Rosiglitazone 162-175 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 252-257 22087241-4 2011 Furthermore, the absence of PGC-1alpha did not prevent the positive effect of rosiglitazone on mitochondrial gene expression or biogenesis, but it precluded the induction by rosiglitazone of UCP1 and other brown fat-specific genes in white adipose tissue. Rosiglitazone 174-187 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 191-195 28240605-5 2017 However, in subcutaneous inguinal fat (iWAT), rosiglitazone markedly induced molecular signatures of brown fat, including the key thermogenic gene Ucp1. Rosiglitazone 46-59 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 147-151 28240605-9 2017 However, when Ucp1 was activated by rosiglitazone, or by iWAT browning in cold-exposed or young mice, expression of the B6 version of Ucp1 was no longer defective relative to the 129 version, indicating epigenomic rescue. Rosiglitazone 36-49 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 14-18 28240819-5 2017 RESULTS: Rosiglitazone treatment in 3T3-L1 adipocytes promoted mitochondrial biogenesis, UCP1 expression, and mitochondrial uncoupling. Rosiglitazone 9-22 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 89-93 24065084-6 2014 Chronic IBMX treatment was indispensable for the enhanced Iso-induced Ucp1 expression, and treatment with additional rosiglitazone (Rosi) for days 0-8 further increased the Ucp1 expression. Rosiglitazone 117-130 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 173-177 24065084-6 2014 Chronic IBMX treatment was indispensable for the enhanced Iso-induced Ucp1 expression, and treatment with additional rosiglitazone (Rosi) for days 0-8 further increased the Ucp1 expression. Rosiglitazone 132-136 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 173-177 21723971-7 2012 Administration of antidiabetic TZD rosiglitazone, which sensitizes cells to insulin and increases adipocyte metabolic functions, significantly increased both, BAT (UCP1, PGC1alpha, Dio2, beta3AR, Prdm16, and FoxC2) and WAT (adiponectin and leptin) gene expression in marrow of normoglycemic C57BL/6 mice, but failed to increase the expression of BAT, but not WAT, gene markers in diabetic mice. Rosiglitazone 35-48 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 164-168 19274054-11 2009 Rosiglitazone increased UCP1 mRNA expression 4.5-fold in the BAT(B) and significantly more, 7.9-fold, in the WAT(B) adipocytes. Rosiglitazone 0-13 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 24-28 17434481-6 2007 RSG ameliorated the mitochondrial Hsp60 expression and induced the expression of UCP-1 in both SC and EP fat. Rosiglitazone 0-3 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 81-86