Obesity-induced upregulation of myocardial endothelin-1 expression is mediated by leptin

Suko Adiarto, Noriaki Emoto, Naoko Iwasa, Mitsuhiro Yokoyama

Research output: Contribution to journalArticlepeer-review

20 Citations (Scopus)


Several studies have shown that leptin, the product of the obese gene, may link obesity with cardiovascular diseases, and in particular with cardiac hypertrophy. In vitro studies suggest that the mechanism by which leptin causes cardiac hypertrophy involves the upregulation of endogenous endothelin-1 (ET-1), a potent vasoconstrictor and mitogen. Whether obesity-associated hyperleptinemia causes an increase in myocardial ET-1 expression in vivo remains unclear. To address this issue, we fed mice with a high-fat diet and analyzed serum levels of ET-1 and ET-1 mRNA in the heart. We found that in mice fed a high-fat diet, serum ET-1, myocardial ET-1, leptin and leptin receptor mRNA were all elevated. In contrast, in leptin-deficient obese (ob/ob) mice, both serum and myocardial ET-1 levels were not higher than in wild type mice. These findings suggest that upregulation of myocardial ET-1 by obesity is mediated by leptin.

Original languageEnglish
Pages (from-to)623-627
Number of pages5
JournalBiochemical and Biophysical Research Communications
Issue number3
Publication statusPublished - 16 Feb 2007


  • Cardiac hypertrophy
  • Endothelin-1
  • Leptin
  • Obesity

Fingerprint Dive into the research topics of 'Obesity-induced upregulation of myocardial endothelin-1 expression is mediated by leptin'. Together they form a unique fingerprint.

Cite this