Atrial natriuretic peptide and leptin interactions in healthy men

Front Endocrinol (Lausanne). 2023 Jun 30:14:1195677. doi: 10.3389/fendo.2023.1195677. eCollection 2023.

Abstract

Introduction: Atrial natriuretic peptide (ANP), a hormone secreted from the heart, controls cardiovascular and renal functions including arterial blood pressure and natriuresis. ANP also exerts metabolic effects in adipose tissue, liver and skeletal muscle, and interacts with the secretion of adipokines. We tested the hypothesis that ANP lowers concentrations of the anorexigenic adipokine leptin in healthy humans in vivo.

Methods: Human ANP or matching placebo was infused intravenously (iv) into healthy men in a controlled clinical trial.

Results: Within 135 minutes of iv ANP infusion, we observed an acute decrease in plasma leptin levels compared to controls. Free fatty acids markedly increased with ANP infusion in vivo, indicating activated lipolysis. In human SGBS adipocytes, ANP suppressed leptin release.

Discussion: The study shows that the cardiac hormone ANP reduces the levels of the anorexigenic adipokine leptin in healthy humans, providing further support for ANP as a cardiomyokine in a heart - adipose tissue axis. (registered in the German Clinical Trials Register and the WHO International Clinical Trials Registry Platform was granted under DRKS00024559).

Keywords: ANP; atrial natriuretic peptide; heart failure; insulin resistance; leptin; lipolysis; obesity.

Publication types

  • Controlled Clinical Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipocytes / metabolism
  • Adipose Tissue / metabolism
  • Atrial Natriuretic Factor* / metabolism
  • Atrial Natriuretic Factor* / pharmacology
  • Humans
  • Leptin* / metabolism
  • Lipolysis
  • Male

Substances

  • Atrial Natriuretic Factor
  • Leptin

Grants and funding

TM received research support from the German Research Foundation (DFG-TRR152 and TRR296). PF-P was supported by the Deutsche Forschungsgemeinschaft – Projektnummer 398707781 – Heisenberg professorship. AB received research support from the German Research Foundation (BI1292/10-1, BI1292/9-1, BI1229/12-1, GRK 2816). This work was funded in part by the German Center for Diabetes Research (DZD, 01GI0925). RJvS receives support from the Helmholtz Association by a Helmholtz Young Investigator Group.