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Updated: May 26, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
08:34

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Published on: June 3, 2016

Axl deficiency does not affect adipogenesis or adipose tissue development.

Ilse Scroyen1, Liesbeth Frederix, H Roger Lijnen

  • 1Center for Molecular and Vascular Biology, Leuven, Belgium.

Obesity (Silver Spring, Md.)
|December 22, 2011
PubMed
Summary

Axl receptor deficiency did not impact adipogenesis in cell cultures or overall body fat in mice. Compensatory mechanisms by related TAM family receptors may explain the lack of significant long-term effects on adiposity.

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Metabolic Research

Background:

  • The Axl receptor tyrosine kinase, a high-affinity receptor for growth arrest-specific protein 6 (GAS6), plays roles in various cellular processes.
  • Its specific involvement in adiposity and metabolic regulation remains incompletely understood.
  • Understanding Axl's function is crucial for metabolic disease research.

Purpose of the Study:

  • To investigate the role of the Axl receptor in adipogenesis and adiposity.
  • To determine if genetic deficiency of Axl affects fat cell differentiation and body weight regulation in mice.
  • To explore potential compensatory mechanisms by other TAM family receptors.

Main Methods:

  • Murine embryonic fibroblasts (MEFs) from Axl-deficient (Axl(-/-)) and wild-type (Axl(+/+)) mice were differentiated into adipocytes.
  • Mice of both genotypes were fed standard fat diet (SFD) or high-fat diet (HFD) for 15 weeks.
  • Adipogenesis was assessed by Oil Red O staining and adipogenic marker expression; body weight, fat mass, adipocyte size, glucose, and insulin tolerance were measured.

Main Results:

  • Axl deficiency did not alter adipocyte differentiation in vitro, evidenced by similar Oil Red O uptake and adipogenic marker expression (aP2, PPARγ).
  • While Axl(-/-) mice showed transiently lower weight gain on HFD early on, overall body weight and fat mass (subcutaneous and gonadal) were comparable between genotypes after 15 weeks.
  • No significant differences in adipocyte size, glucose homeostasis, or insulin tolerance were observed between Axl(-/-) and Axl(+/+) mice.

Conclusions:

  • Axl receptor deficiency does not significantly affect adipogenesis in vitro or in vivo.
  • The absence of Axl's effect on adiposity may be due to compensatory roles of other TAM family receptors, such as Mer and Tyro3.
  • Axl does not appear to be a critical regulator of overall adiposity or glucose metabolism in this model.