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TranscriptomicsPPAR Controls Gene Expression in MSC Cells
Rosiglitazone (Rosi), a member of the thiazolidinedione class of drugs used to treat type 2 diabetes, activates the adipocyte-specific transcription factor peroxisome proliferator-activated receptor gamma (PPARg). This activation causes bone loss in animals and humans, at least in part due to suppre...
ORGANISM(S): Mus musculus 
2009-01-15 | E-GEOD-10192 | biostudies-arrayexpress
TranscriptomicsMuscle Involvement in Preservation of Metabolic Flexibility by Treatment using n-3 PUFA or Rosiglitazone in Dietary-Obese Mice
Impaired resistance to insulin, the key defect in type 2 diabetes (T2D), is associated with a low capacity to adapt fuel oxidation to fuel availability, i.e., metabolic inflexibility. The hampered metabolic adaptability triggers a further damage of insulin signaling. Since skeletal muscle is the mai...
ORGANISM(S): Mus musculus 
2012-09-07 | E-GEOD-36716 | biostudies-arrayexpress
TranscriptomicsMuscle Involvement in Preservation of Metabolic Flexibility by a Combination Treatment using n-3 PUFA and Rosiglitazone in Dietary-Obese Mice
Impaired resistance to insulin, the key defect in type 2 diabetes (T2D), is associated with a low capacity to adapt fuel oxidation to fuel availability, i.e., metabolic inflexibility. The hampered metabolic adaptability triggers a further damage of insulin signaling. Since skeletal muscle is the mai...
ORGANISM(S): Mus musculus 
2012-09-07 | E-GEOD-36717 | biostudies-arrayexpress
TranscriptomicsAntidiabetic Rosiglitazone Remodels the Adipocyte Transcriptome by Redistributing Transcription to PPARg-Driven Enhancers [HTS]
Rosiglitazone (rosi) is a powerful insulin sensitizer, but serious toxicities have curtailed its widespread clinical use. Rosi functions as a high-affinity ligand for PPARg, the adipocyte-predominant nuclear receptor (NR). The classic model, involving binding of ligand to the NR on DNA, explains p...
ORGANISM(S): Mus musculus 
2014-05-02 | E-GEOD-56745 | biostudies-arrayexpress
TranscriptomicsMuscle Involvement in Preservation of Metabolic Flexibility by a Combination Treatment using n-3 PUFA and Rosiglitazone in Dietary-Obese Mice
Impaired resistance to insulin, the key defect in type 2 diabetes (T2D), is associated with a low capacity to adapt fuel oxidation to fuel availability, i.e., metabolic inflexibility. The hampered metabolic adaptability triggers a further damage of insulin signaling. Since skeletal muscle is the mai...
ORGANISM(S): Mus musculus 
2012-09-07 | GSE36717 | GEO
TranscriptomicsMuscle Involvement in Preservation of Metabolic Flexibility by Treatment using n-3 PUFA or Rosiglitazone in Dietary-Obese Mice
Impaired resistance to insulin, the key defect in type 2 diabetes (T2D), is associated with a low capacity to adapt fuel oxidation to fuel availability, i.e., metabolic inflexibility. The hampered metabolic adaptability triggers a further damage of insulin signaling. Since skeletal muscle is the mai...
ORGANISM(S): Mus musculus 
2012-09-07 | GSE36716 | GEO
UnknownNear full-length sequence analysis of HIV type 1 BF recombinants from Italy.
Not available
S-EPMC3292755 | biostudies-literature
UnknownA Versatile Top-Down Patterning Technique for Perovskite On-Chip Integration.
Not available
S-EPMC12392744 | biostudies-literature
UnknownUnmasking differential effects of rosiglitazone and pioglitazone in the combination treatment with n-3 fatty acids in mice fed a high-fat diet.
Not available
S-EPMC3207833 | biostudies-literature
UnknownPreservation of metabolic flexibility in skeletal muscle by a combined use of n-3 PUFA and rosiglitazone in dietary obese mice.
Not available
S-EPMC3432031 | biostudies-literature
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