Clusterin/ApoJ enhances central leptin signaling through Lrp2-mediated endocytosis

EMBO Rep. 2014 Jul;15(7):801-8. doi: 10.15252/embr.201338317. Epub 2014 May 12.

Abstract

Hypothalamic leptin signaling plays a central role in maintaining body weight homeostasis. Here, we show that clusterin/ApoJ, recently identified as an anorexigenic neuropeptide, is an important regulator in the hypothalamic leptin signaling pathway. Coadministration of clusterin potentiates the anorexigenic effect of leptin and boosts leptin-induced hypothalamic Stat3 activation. In cultured neurons, clusterin enhances receptor binding and subsequent endocytosis of leptin. These effects are mainly mediated through the LDL receptor-related protein-2 (Lrp2). Notably, inhibition of hypothalamic clusterin, Lrp2 or endocytosis abrogates anorexia and hypothalamic Stat3 activation caused by leptin. These findings propose a novel regulatory mechanism in central leptin signaling pathways.

Keywords: Lrp2; Stat3; clusterin; endocytosis; leptin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Clusterin / deficiency
  • Clusterin / genetics
  • Clusterin / metabolism*
  • Endocytosis / physiology*
  • Hypothalamus / metabolism
  • Leptin / metabolism*
  • Low Density Lipoprotein Receptor-Related Protein-2 / metabolism*
  • Male
  • Mice
  • Mice, Knockout
  • Neurons / metabolism
  • Protein Binding
  • Receptors, Leptin / metabolism
  • Signal Transduction*

Substances

  • Clusterin
  • Leptin
  • Low Density Lipoprotein Receptor-Related Protein-2
  • Receptors, Leptin