Abstract

The past several years have seen an explosive increase in our understanding of the transcriptional basis of adipose cell differentiation. In particular, a key role has been illustrated for PPAR-gamma, a member of the nuclear hormone receptor superfamily. PPAR-gamma has also been recently identified as the major functional receptor for the thiazolidinedione class of insulin-sensitizing drugs. This review examines the evidence that has implicated this transcription factor in the processes of adipogenesis and systemic insulin action. In addition, several models are discussed that may explain how a single protein can be involved in these related but distinct physiological actions. I also point out several important areas where our knowledge is incomplete and more research is needed. Finally, I discuss how advances in our understanding of nuclear receptor function, particularly the docking of cofactors in a ligand-dependent fashion, should lead to improved drugs that utilize the PPAR-gamma system for the treatment of insulin resistance.

Keywords

AdipogenesisNuclear receptorThiazolidinedionePeroxisome proliferator-activated receptorTranscription factorRegulatorReceptorBiologyInsulin resistanceAdipose tissueCell biologyInsulinEndocrinologyType 2 diabetesGeneticsGeneDiabetes mellitus

Affiliated Institutions

Related Publications

Publication Info

Year
1998
Type
review
Volume
47
Issue
4
Pages
507-514
Citations
1732
Access
Closed

External Links

Social Impact

Social media, news, blog, policy document mentions

Citation Metrics

1732
OpenAlex

Cite This

Bruce M. Spiegelman (1998). PPAR-gamma: adipogenic regulator and thiazolidinedione receptor.. Diabetes , 47 (4) , 507-514. https://doi.org/10.2337/diabetes.47.4.507

Identifiers

DOI
10.2337/diabetes.47.4.507