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Cardiac peroxisome-proliferator-activated receptor expression in hypertension co-existing with diabetes

Ting-I Lee1, Yu-Hsun Kao, Yao-Chang Chen

  • 1Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, and Wan Fang Hospital, Taiwan.

Clinical Science (London, England : 1979)
|April 20, 2011
PubMed

Insights

Diabetes and hypertension alter heart PPAR isoform expression, with rosiglitazone treatment mitigating these effects. This study explores how these conditions impact myocardial PPARs and inflammation.

Area of Science:

  • Cardiovascular Research
  • Endocrinology
  • Molecular Biology

Background:

  • Hypertension and diabetes mellitus (DM) frequently coexist and can negatively impact heart function.
  • The specific effects of DM and peroxisome-proliferator-activated receptor (PPAR)-γ agonists on hypertensive myocardium are not well understood.
  • PPAR-γ agonists, such as rosiglitazone (RGZ), have potential roles in cardiovascular health and disease.

Purpose of the Study:

  • To investigate how DM and a PPAR-γ agonist (RGZ) modulate the effects of hypertension on myocardial expression of PPAR isoforms.
  • To assess the impact of DM and RGZ on cardiac inflammation markers and oxidative stress in a hypertensive model.
  • To elucidate the interplay between hypertension, DM, PPARs, and cardiac function.

Main Methods:

  • Utilized spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) rats, including diabetic models and those treated with RGZ.
  • Quantified cardiac PPAR isoforms (α, δ, γ) mRNA and protein levels using real-time PCR and Western blotting.
  • Assessed cardiac NADPH oxidase activity and levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6).

Main Results:

  • Hypertension in SHRs led to decreased PPAR-α and PPAR-δ but increased PPAR-γ expression.
  • Diabetes exacerbated these hypertension-induced changes in PPAR isoform expression.
  • RGZ treatment attenuated the detrimental effects of DM and hypertension on PPAR expression and reduced cardiac TNF-α, IL-6, and NADPH oxidase activity.

Conclusions:

  • Diabetes and PPAR-γ agonists significantly modulate the effects of hypertension on cardiac PPAR isoform expression.
  • RGZ demonstrates a protective effect by normalizing PPAR expression and reducing inflammation and oxidative stress in the hypertensive and diabetic heart.
  • These findings highlight the complex interactions between metabolic and hypertensive conditions on cardiac molecular pathways.

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