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Updated: May 26, 2026
Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
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.
Abstract:
To evaluate a potential role of Axl, the high-affinity receptor of growth arrest-specific protein 6 (GAS6) in adiposity, murine embryonic fibroblasts (MEF) derived from mice with genetic deficiency of Axl (Axl(-/-)) or wild-type littermates (Axl(+/+)) were differentiated into mature adipocytes. In addition, Axl(-/-) and Axl(+/+) mice were kept on standard fat diet (SFD) or on high-fat diet (HFD) for 15 weeks. Deficiency of Axl in MEF did not affect differentiation, as shown by a similar uptake of Oil Red O and expression of the adipogenic markers aP2 and peroxisome proliferator activator receptor γ (PPARγ) at the end of the differentiation. In the first 7 weeks of HFD feeding, Axl(-/-) mice gained less weight than their wild-type littermates. Weight gain for both genotypes on either SFD of HFD over 15 weeks was, however, not significantly different, resulting in comparable body weights, as well as subcutaneous (s.c.) and gonadal (GON) fat mass. Adipocyte size in the fat tissues was not affected by Axl deficiency. Gene expression analysis indicated that the absence of Axl in vivo may be compensated for by the other TAM family members Mer and Tyro3. Glucose and insulin tolerance tests (ITT) in Axl(-/-) and Axl(+/+) mice did not reveal significant differences in glucose homeostasis. Thus, Axl deficiency had no significant effect on adipogenesis in vitro or in vivo.
Insights
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.
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.
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