ArticlePloS one2011
Rosiglitazone-induced mitochondrial biogenesis in white adipose tissue is independent of peroxisome proliferator-activated receptor γ coactivator-1α.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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Who cites it
37 citing papers in PubMed, 86 citations in OpenAlex.
- Dual Modulation of Adipogenesis and Apoptosis by PPARG Agonist Rosiglitazone and Antagonist Betulinic Acid in 3T3-L1 Cells.Biomedicines · 2025Article
- Mito-Modulatory Medication Use and Skeletal Muscle Bioenergetics Among Older Men and Women: The Study of Muscle, Mobility, and Aging.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025Article
- Brd9 antagonism induces beige adipocytes in white adipose tissues and protects against diet-induced obesity.Obesity (Silver Spring, Md.) · 2025Article
- Obesity-induced PARIS (ZNF746) accumulation in adipose progenitor cells leads to attenuated mitochondrial biogenesis and impaired adipogenesis.Scientific reports · 2023Article
- Intestinal Pgc1α ablation protects from liver steatosis and fibrosis.JHEP reports : innovation in hepatology · 2023Article
- Methylmalonic Acid Impairs Cell Respiration and Glutamate Uptake in C6 Rat Glioma Cells: Implications for Methylmalonic Acidemia.Cellular and molecular neurobiology · 2023Article
- Many Ways to Rome: Exercise, Cold Exposure and Diet-Do They All Affect BAT Activation and WAT Browning in the Same Manner?International journal of molecular sciences · 2022Review
- Brown Adipose Tissue and Novel Management Strategies for Polycystic Ovary Syndrome Therapy.Frontiers in endocrinology · 2022Review
- Mitofusion is required for MOTS-c induced GLUT4 translocation.Scientific reports · 2021Article
- Indomethacin promotes browning and brown adipogenesis in both murine and human fat cells.Pharmacology research & perspectives · 2020Article
- PPARγ and PPARα synergize to induce robust browning of white fat in vivo.Molecular metabolism · 2020Article
- Rosiglitazone Protects Endothelial Cells From Irradiation-Induced Mitochondrial Dysfunction.Frontiers in pharmacology · 2020Article
- The Role of Adipose Tissue Mitochondria: Regulation of Mitochondrial Function for the Treatment of Metabolic Diseases.International journal of molecular sciences · 2019Review
- PGC-1α activation: a therapeutic target for type 2 diabetes?Eating and weight disorders : EWD · 2019Review
- Article
- Reprogramming of basic metabolic pathways in microbial sepsis: therapeutic targets at last?EMBO molecular medicine · 2018Review
- The Implication of PGC-1α on Fatty Acid Transport across Plasma and Mitochondrial Membranes in the Insulin Sensitive Tissues.Frontiers in physiology · 2017Review
- Development of Therapeutics That Induce Mitochondrial Biogenesis for the Treatment of Acute and Chronic Degenerative Diseases.Journal of medicinal chemistry · 2016Review
- Skeletal muscle mitochondrial health and spinal cord injury.World journal of orthopedics · 2016Review
- Dual Outcomes of Rosiglitazone Treatment on Fatty Liver.The AAPS journal · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThiazolidinediones, a family of insulin-sensitizing drugs commonly used to treat type 2 diabetes, are thought to exert their effects in part by promoting mitochondrial biogenesis in white adipose tissue through the transcriptional coactivator PGC-1α (Peroxisome Proliferator-Activated Receptor γ Coactivator-1α). METHODOLOGY/PRINCIPAL
findingsTo assess the role of PGC-1α in the control of rosiglitazone-induced mitochondrial biogenesis, we have generated a mouse model that lacks expression of PGC-1α specifically in adipose tissues (PGC-1α-FAT-KO mice). We found that expression of genes encoding for mitochondrial proteins involved in oxidative phosphorylation, tricarboxylic acid cycle or fatty acid oxidation, was similar in white adipose tissue of wild type and PGC-1α-FAT-KO mice. Furthermore, the absence of PGC-1α 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. Consistent with the in vivo findings, basal and rosiglitazone-induced mitochondrial gene expression in 3T3-L1 adipocytes was unaffected by the knockdown of PGC-1α but it was impaired when PGC-1β expression was knockdown by the use of specific siRNA. CONCLUSIONS/SIGNIFICANCE: These results indicate that in white adipose tissue PGC-1α is dispensable for basal and rosiglitazone-induced mitochondrial biogenesis but required for the rosiglitazone-induced expression of UCP1 and other brown adipocyte-specific markers. Our study suggests that PGC-1α is important for the appearance of brown adipocytes in white adipose tissue. Our findings also provide evidence that PGC-1β and not PGC-1α regulates basal and rosiglitazone-induced mitochondrial gene expression in white adipocytes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.