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Related Experiment Video

Updated: Apr 15, 2026

A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging
09:37

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ADAMTS13 deficiency in mice does not affect adipose tissue development.

Lotte Geys1, Ilse Scroyen1, Elien Roose2

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

Biochimica Et Biophysica Acta
|March 28, 2015
PubMed
Summary

This study found that the protein ADAMTS13 (A Disintegrin and Metalloproteinase with Thrombospondin type 1 motif, member 13) does not play a direct role in obesity development or associated inflammation in mice. Further research is needed to understand its role in thrombotic thrombocytopenic purpura (TTP).

Keywords:
ADAMTS13Adipose tissueMiceObesity

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Area of Science:

  • Biochemistry
  • Physiology
  • Metabolic Diseases

Background:

  • Body Mass Index (BMI) correlates positively with ADAMTS13 levels in humans.
  • Obesity development involves angiogenesis and inflammation, with increased hepatic ADAMTS13 synthesis.

Purpose of the Study:

  • To investigate the functional role of ADAMTS13 in adiposity, angiogenesis, and inflammation using a mouse model.
  • To resolve the apparent contradiction between increased ADAMTS13 in obesity and its role in thrombotic thrombocytopenic purpura (TTP).

Main Methods:

  • Male wild-type (WT) and ADAMTS13-deficient (Adamts13-/-) mice were fed either a standard chow (SFD) or a high-fat diet (HFD) for 15 weeks.
  • Evaluated body weight gain, adipose tissue mass, adipocyte size, and density.
  • Assessed mRNA expression of adipogenic, endothelial, inflammatory, and oxidative stress markers.
  • Analyzed metabolic parameters, glucose tolerance, and insulin tolerance tests.

Main Results:

  • High-fat diet (HFD) significantly increased ADAMTS13 antigen and activity in WT mice.
  • ADAMTS13 deficiency did not affect body weight, adipose tissue mass, or adipocyte size.
  • Obese Adamts13-/- mice exhibited higher adipocyte density and lower blood vessel density in gonadal fat compared to obese WT mice.
  • No significant differences in metabolic parameters, glucose, or insulin tolerance were observed between obese genotypes, except for higher adiponectin and cholesterol in obese Adamts13-/- mice.

Conclusions:

  • ADAMTS13 does not appear to have a functional role in promoting adiposity, angiogenesis, or inflammation in mice.
  • The findings suggest ADAMTS13 does not directly contribute to adipose tissue development.
  • Further investigation is warranted to clarify the relationship between ADAMTS13, obesity, and TTP risk.