Both overexpression of agouti-related peptide or neuropeptide Y in the paraventricular nucleus or lateral hypothalamus induce obesity in a neuropeptide- and nucleus specific manner

Eur J Pharmacol. 2011 Jun 11;660(1):148-55. doi: 10.1016/j.ejphar.2010.12.021. Epub 2011 Jan 3.

Abstract

Both reduction of melanocortin signaling and increase in neuropeptide Y signaling in the brain result in obesity. However, where in the brain reduced melanocortin or increased neuropeptide Y signaling mediate these effects is poorly understood. In separate experiments we have injected recombinant adeno-associated viral vectors that overexpressed agouti-related peptide or neuropeptide Y in specific brain regions namely the paraventricular nucleus and the lateral hypothalamus. In this review we compare the results from these studies and discuss these data with previous data from intracerebroventricular or local brain injections. This review shows that the effects of agouti-related peptide clearly differ from those of neuropeptide Y. In addition, these data suggests complementary roles for these neuropeptides in energy balance.

Publication types

  • Review

MeSH terms

  • Agouti-Related Protein / genetics*
  • Agouti-Related Protein / metabolism
  • Animals
  • Gene Expression
  • Humans
  • Hypothalamic Area, Lateral / metabolism*
  • Neuropeptide Y / genetics*
  • Neuropeptide Y / metabolism
  • Obesity / genetics*
  • Obesity / metabolism
  • Obesity / physiopathology
  • Organ Specificity
  • Paraventricular Hypothalamic Nucleus / metabolism*
  • Peptide Fragments / genetics*
  • Peptide Fragments / metabolism

Substances

  • Agouti-Related Protein
  • Neuropeptide Y
  • Peptide Fragments
  • agouti-related peptide, (Yc(CRFFNAFC)Y)