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Related Experiment Videos

Leptin receptor action in hepatic cells

Y Wang1, K K Kuropatwinski, D W White

  • 1Department of Molecular and Cellular Biology, Roswell Park Cancer Institute, Buffalo, New York 14263, USA.

The Journal of Biological Chemistry
|June 27, 1997
PubMed
Summary

Leptin

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cell Signaling

Background:

  • Leptin is a key hormone regulating body weight homeostasis.
  • Two main leptin receptor (OB-R) forms exist: short (OB-RS) and long (OB-RL).
  • OB-RL signaling resembles that of interleukin (IL)-6 type-cytokine receptors.

Purpose of the Study:

  • To investigate OB-R gene induction specificity.
  • To define OB-R cooperation with other signaling pathways.
  • To characterize OB-RL function in hepatic cells.

Main Methods:

  • Generation of stable rat and human hepatoma cell lines expressing human OB-RL.
  • Analysis of leptin binding and IL-6 receptor-like signaling.
  • Assessment of STAT protein activation, acute-phase protein induction, and cytokine synergism.
  • Investigation of phosphatidylinositol 3-kinase recruitment to insulin receptor substrate-2.

Main Results:

  • Hepatoma cells expressing OB-RL showed enhanced leptin binding.
  • Leptin activated STAT proteins and induced acute-phase proteins, similar to IL-6.
  • Leptin synergized with IL-1 and tumor necrosis factor-alpha.
  • Leptin mediated phosphatidylinositol 3-kinase recruitment to insulin receptor substrate-2 but did not affect insulin signaling.

Conclusions:

  • OB-RL in hepatic cells functions analogously to the IL-6 receptor.
  • Leptin does not appear to interfere with insulin action in hepatoma cells.
  • Leptin's role in obesity-associated diabetes symptoms may not involve direct modulation of hepatic insulin signaling.

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