PPARγ Agonist Beyond Glucose Lowering Effect

Akira Sugawara, Akira Uruno, Masataka Kudo, Ken Matsuda, Chul Woo Yang, Sadayoshi Ito

Research output: Contribution to journalArticlepeer-review

16 Citations (Scopus)


The nuclear hormone receptor PPARγ is activated by several agonists, including members of the thiazolidinedione group of insulin sensitizers. Pleiotropic beneficial effects of these agonists, independent of their blood glucose- lowering effects, have recently been demonstrated in the vasculature. PPARγ agonists have been shown to lower blood pressure in animals and humans, perhaps by suppressing the renin-angiotensin (Ang)-aldosterone system (RAAS), including the inhibition of Ang II type 1 receptor expression, Ang-II-mediated signaling pathways, and Ang-II-induced adrenal aldosterone synthesis/secretion. PPARγ agonists also inhibit the progression of atherosclerosis in animals and humans, possibly through a pathway involving the suppression of RAAS and the thromboxane A2 system, as well as the protection of endothelial function. Moreover, PPARγ-agonist-mediated renal protection, especially the reduction of albuminuria, has been observed in diabetic nephropathy, including animal models of the disease, and in non-diabetic renal dysfunction. The renal protective activities may reflect, at least in part, the ability of PPARγ agonists to lower blood pressure, protect endothelial function, and cause vasodilation of the glomerular efferent arterioles. Additionally, anti-neoplastic effects of PPARγ agonists have recently been described. Based on the multiple therapeutic actions of PPARγ agonists, they will no doubt lead to novel approaches in the treatment of lifestyle-related and other diseases.

Original languageEnglish
Pages (from-to)19-24
Number of pages6
JournalKorean Journal of Internal Medicine
Issue number1
Publication statusPublished - 2011 Mar


  • Angiotensin II
  • Endothelium
  • Kidney
  • Thiazolidinediones
  • Thromboxane

ASJC Scopus subject areas

  • Internal Medicine


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