Advertisement

Atrial Natriuretic Peptide Induces Postprandial Lipid Oxidation in Humans

  1. Andreas L. Birkenfeld12,
  2. Petra Budziarek1,
  3. Michael Boschmann1,
  4. Cedric Moro3,
  5. Frauke Adams1,
  6. Gabriele Franke1,
  7. Michel Berlan3,
  8. Marie A. Marques3,
  9. Fred C.G.J. Sweep4,
  10. Friedrich C. Luft1,
  11. Max Lafontan3 and
  12. Jens Jordan5
  1. 1Experimental and Clinical Research Center, Charité and HELIOS-Klinikum, Berlin, Germany
  2. 2Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut
  3. 3Institut National de la Santé et de la Recherche Médicale, Unité 858, Institut de Médecine Moléculaire de Rangueil, Université Paul Sabatier, Toulouse, France
  4. 4Department of Chemical Endocrinology, Radboud University Nijmegen Medical Centre, Nijmegen, the Netherlands
  5. 5Institute of Clinical Pharmacology, Hannover Medical School, Hannover, Germany
  1. Corresponding author: Jens Jordan, jordan.jens{at}mh-hannover.de

Abstract

OBJECTIVE—Atrial natriuretic peptide (ANP) regulates arterial blood pressure. In addition, ANP has recently been shown to promote human adipose tissue lipolysis through cGMP-mediated hormone-sensitive lipase activation. We hypothesized that ANP increases postprandial free fatty acid (FFA) availability and energy expenditure while decreasing arterial blood pressure.

RESEARCH DESIGN AND METHODS—We infused human ANP (25 ng · kg−1 · min−1) in 12 men (age 32 ± 0.8 years, BMI 23.3 ± 0.4 kg/m2) before, during, and 2 h after ingestion of a standardized high-fat test meal in a randomized, double-blind, cross-over fashion. Cardiovascular changes were monitored by continuous electrocardiogram and beat-by-beat blood pressure recordings. Metabolism was monitored through venous blood sampling, intramuscular and subcutaneous abdominal adipose tissue microdialysis, and indirect calorimetry.

RESULTS—ANP infusion decreased mean arterial blood pressure by 4 mmHg during the postprandial phase (P < 0.01 vs. placebo). At the same time, ANP induced lipolysis systemically (P < 0.05 vs. placebo) and locally in subcutaneous abdominal adipose tissue (P < 0.0001 vs. placebo), leading to a 50% increase in venous glycerol (P < 0.01) and FFA (P < 0.05) concentrations compared with placebo. The increase in FFA availability with ANP was paralleled by a 15% increase in lipid oxidation rates (P < 0.05 vs. placebo), driving a substantial increase in postprandial energy expenditure (P < 0.05 vs. placebo).

CONCLUSIONS—Our data identify the ANP system as a novel pathway regulating postprandial lipid oxidation, energy expenditure, and concomitantly arterial blood pressure. The findings could have therapeutic implications.

Footnotes

  • Published ahead of print at http://diabetes.diabetesjournals.org on 3 October 2008.

    A.L.B. and P.B. contributed equally to this work.

    Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

    The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

    • Accepted September 16, 2008.
    • Received May 15, 2008.
| Table of Contents

This Article

  1. Diabetes December 2008 vol. 57 no. 12 3199-3204
  1. » Abstract
  2. All Versions of this Article:
    1. db08-0649v1
    2. 57/12/3199 most recent

Social Bookmarking

Advertisement