Insights into amylin-leptin synergy

Trends Endocrinol Metab. 2010 Aug;21(8):473-9. doi: 10.1016/j.tem.2010.03.006. Epub 2010 Apr 21.


Although the adipokine leptin is regarded as the prototypical long-term signal of energy balance, obese individuals are largely nonresponsive to exogenous leptin administration. Restoration of leptin responsiveness in obesity has been elusive despite a detailed understanding of the molecular mechanisms of leptin signaling. Recent translational research findings point to a potential therapeutic approach that incorporates amylin (a beta-cell hormone) and leptin agonism, with amylin restoring or enhancing leptin sensitivity. Here we hypothesize various physiological, neurobiological and molecular mechanisms that could mediate the interaction of these two neurohormonal signals and discuss several methodological challenges. Understanding how amylin agonism improves leptin function could point to general therapeutic strategies for combating leptin resistance and associated obesity.

Publication types

  • Review

MeSH terms

  • Animals
  • Body Weight / drug effects
  • Drug Synergism
  • Humans
  • Hypothalamus / drug effects
  • Islet Amyloid Polypeptide / pharmacology*
  • Islet Amyloid Polypeptide / physiology*
  • Islet Amyloid Polypeptide / therapeutic use
  • Leptin / pharmacology*
  • Leptin / physiology*
  • Leptin / therapeutic use
  • Obesity / drug therapy*
  • Obesity / physiopathology
  • Rhombencephalon / drug effects


  • Islet Amyloid Polypeptide
  • Leptin