Monomeric TRAP Induces Insulin Sensitive Obesity
Author Information
Author(s): Lång Pernilla, van Harmelen Vanessa, Rydén Mikael, Kaaman Maria, Parini Paolo, Carneheim Claes, Cassady A. Ian, Hume David A., Andersson Göran, Arner Peter
Primary Institution: Karolinska Institutet, Karolinska University Hospital, Huddinge, Sweden
Hypothesis
Does monomeric tartrate-resistant acid phosphatase (TRAP) influence obesity through its effects on adipocyte precursor cells?
Conclusion
Monomeric TRAP, secreted from adipose tissue macrophages, induces hyperplastic obesity while maintaining normal adipocyte lipid metabolism and insulin sensitivity.
Supporting Evidence
- Over-expression of monomeric TRAP in mice led to early onset spontaneous hyperplastic obesity.
- Monomeric TRAP was highly expressed in the adipose tissue of obese individuals.
- TRAP over-expressing mice exhibited signs of low-grade inflammation without abnormal adipocyte metabolism.
Takeaway
Some cells in fat can make a protein called TRAP that helps create more fat cells without making them bigger, which can lead to obesity but still keep the body working well with insulin.
Methodology
The study used transgenic mice overexpressing monomeric TRAP and human adipose tissue samples to analyze the effects of TRAP on adipocyte proliferation and differentiation.
Potential Biases
Potential bias in the selection of animal models and human subjects may affect the generalizability of the results.
Limitations
The study's findings may not fully translate to humans due to differences in metabolism and fat cell biology.
Participant Demographics
The study included both male and female mice and human subjects with varying body mass indices.
Statistical Information
P-Value
p=0.003
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
Want to read the original?
Access the complete publication on the publisher's website