Control of lipolysis by natriuretic peptides and cyclic GMP

Trends Endocrinol Metab. May-Jun 2008;19(4):130-7. doi: 10.1016/j.tem.2007.11.006. Epub 2008 Mar 11.

Abstract

Human fat cell lipolysis was, until recently, thought to be mediated exclusively by a cAMP-dependent protein kinase (PKA)-regulated pathway under the control of catecholamines and insulin. We have shown that atrial- and B-type natriuretic peptides (ANP and BNP respectively) stimulate lipolysis in human fat cells through a cGMP-dependent protein kinase (PKG) signaling pathway independent of cAMP production and PKA activity. Pharmacological or physiological (exercise) increases in plasma ANP levels stimulate lipid mobilization in humans. This pathway becomes important during chronic treatment with beta-adrenoceptor antagonists, which inhibit catecholamine-induced lipolysis but enhance cardiac ANP release. These findings have metabolic implications and point to potential problems when natriuretic peptide secretion is altered or during therapeutic use of recombinant BNP.

Publication types

  • Review

MeSH terms

  • Adipose Tissue / drug effects
  • Adipose Tissue / metabolism
  • Animals
  • Biomarkers / analysis
  • Cyclic GMP / pharmacology*
  • Humans
  • Lipolysis / drug effects*
  • Lipolysis / physiology
  • Models, Biological
  • Natriuretic Peptides / pharmacology*

Substances

  • Biomarkers
  • Natriuretic Peptides
  • Cyclic GMP