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Published on: November 14, 2013
SPARC-null mice exhibit increased adiposity without significant differences in overall body weight
A D Bradshaw1, D C Graves, K Motamed
1Department of Vascular Biology, Hope Heart Institute, Seattle, WA 98104, USA.
Summary
Secreted protein acidic and rich in cysteine (SPARC) deficiency in mice leads to increased adipose tissue accumulation. SPARC absence results in larger adipocytes and more numerous fat cells, suggesting SPARC limits fat tissue growth.
Area of Science:
- Biochemistry
- Cell Biology
- Physiology
Background:
- Secreted protein acidic and rich in cysteine (SPARC) is an extracellular matrix (ECM) protein influencing cell behavior and ECM synthesis.
- SPARC deficiency in mice causes ECM abnormalities, cataracts, osteopenia, and rapid wound healing.
- SPARC-null mice exhibit altered adipose tissue characteristics.
Purpose of the Study:
- To investigate the role of SPARC in adipose tissue regulation.
- To determine the impact of SPARC absence on adipocyte size, number, and ECM composition.
- To explore the potential mechanisms by which SPARC affects fat accumulation.
Main Methods:
- Comparison of adipose tissue from SPARC-null and wild-type mice.
- Analysis of adipocyte size and number in epididymal fat pads.
- Assessment of collagen I levels in adipose tissue.
- Quantification of SPARC mRNA in stromal/vascular and adipocyte fractions.
Main Results:
- SPARC-null mice showed increased subcutaneous fat deposits and larger epididymal fat pads.
- Reduced collagen I content was observed in SPARC-null fat pads.
- SPARC-null mice had significantly larger adipocyte diameters and increased adipocyte numbers.
- Elevated serum leptin levels were noted in SPARC-null mice without significant body weight differences.
Conclusions:
- SPARC absence leads to increased adipose tissue mass due to enhanced adipocyte size and number.
- SPARC may limit adipose tissue accumulation by regulating adipocyte shape and ECM production.
- These findings highlight SPARC's role in metabolic regulation and adipose tissue homeostasis.

