PPARγ signaling and metabolism: the good, the bad and the future
By Maryam Ahmadian, J. M. Suh, N. Hah, C. Liddle, A. Atkins, M. Downes, R. Evans. Nature Medicine, 2013
1,918 citations recorded by the source corpus.
Thiazolidinediones (TZDs) are potent insulin sensitizers that act through the nuclear receptor peroxisome proliferator-activated receptor-γ (PPARγ) and are highly effective oral medications for type 2 diabetes. However, their unique benefits are shadowed by the risk for fluid retention, weight gain, bone loss and congestive heart failure. This raises the question as to whether it is possible to build a safer generation of PPARγ-specific drugs that evoke fewer side effects while preserving insulin-sensitizing potential. Recent studies that have supported the continuing physiologic and therapeutic relevance of the PPARγ pathway also provide opportunities to develop newer classes of molecules that reduce or eliminate adverse effects. This review highlights key advances in understanding PPARγ signaling in energy homeostasis and metabolic disease and also provides new explanations for adverse events linked to TZD-based therapy.
Subfields: Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/5af9ad4fab2ecf1a9e4bc99ac46d0b8766beeef2
Citations in the corpus
- Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal (2014, neutral): “Mario F. Muñoz was supported by Consejeria de Economı́a, Innovacion y Ciencia de la Junta de Andalucia (Spain) postdoctoral fellowship (P10-CTS-6494).”
- NAFLD and increased risk of cardiovascular disease: clinical associations, pathophysiological mechanisms and pharmacological implications (2020, neutral): “111 Glitazones (eg, rosiglitazone and pioglitazone) are selective activators of PPAR-γ and pioglitazone is a potent insulin sensitizer that is currently licensed for treatment of T2DM.”