32
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      The role of neuropeptide Y in the antiobesity action of the obese gene product.

      Nature

      Animals, Body Weight, Cell Membrane, metabolism, Diabetes Mellitus, Experimental, Eating, Escherichia coli, Humans, Hypothalamus, physiology, In Vitro Techniques, Leptin, Mice, Neuropeptide Y, Obesity, genetics, Proteins, Rats, Recombinant Proteins, pharmacology

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Recently Zhang et al. cloned a gene that is expressed only in adipose tissue of the mouse. The obese phenotype of the ob/ob mouse is linked to a mutation in the obese gene that results in expression of a truncated inactive protein. Human and rat homologues for this gene are known. Previous experiments predict such a hormone to have a hypothalamic target. Hypothalamic neuropeptide Y stimulates food intake, decreases thermogenesis, and increases plasma insulin and corticosterone levels making it a potential target. Here we express the obese protein in Escherichia coli and find that it suppresses food intake and decreases body weight dramatically when administered to normal and ob/ob mice but not db/db (diabetic) mice, which are thought to lack the appropriate receptor. High-affinity binding was detected in the rat hypothalamus. One mechanism by which this protein regulated food intake and metabolism was inhibition of neuropeptide-Y synthesis and release.

          Related collections

          Author and article information

          Journal
          7566151
          10.1038/377530a0

          Comments

          Comment on this article