ADAMTS13 deficiency in mice does not affect adipose tissue development

• ADAMTS13 antigen and activity levels are higher in plasma of obese versus lean mice.
• There is no functional role of ADAMTS13 in adipose tissue development.
• Angiogenesis in obese adipose tissue is not affected by ADAMTS13 deficiency.
• ADAMTS13 deficiency does not affect inflammation in obese adipose tissue.

BackgroundBMI and ADAMTS13 levels are positively correlated in man. Development of obesity is associated with angiogenesis and inflammation, and increased ADAMTS13 synthesis in the liver.MethodsMale wild-type (WT) and ADAMTS13 deficient (Adamts13−/−) mice were kept on normal chow (SFD) or high fat diet (HFD) for 15 weeks.ResultsHFD feeding of WT mice resulted in significantly enhanced levels of ADAMTS13 antigen and activity as compared to SFD feeding. ADAMTS13 deficiency had no significant effect on body weight gain, subcutaneous (SC) or gonadal (GN) adipose tissue mass, or on adipocyte size. In GN fat of obese (HFD) Adamts13−/− mice, adipocyte density was higher and blood vessel density lower as compared to obese WT mice. No marked effects of genotype were observed on mRNA expression of adipogenic, endothelial, inflammatory or oxidative stress markers in adipose tissue. Analysis of metabolic parameters and of glucose and insulin tolerance did not reveal significant differences between both obese genotypes, except for higher adiponectin and cholesterol levels in obese Adamts13−/− as compared to WT mice.ConclusionOur data do not support a functional role of ADAMTS13 in adiposity nor in associated angiogenesis or inflammation in mice.General significanceADAMTS13 deficiency may cause thrombotic thrombocytopenic purpura (TTP). Obesity, which is associated with enhanced ADAMTS13 levels is nevertheless considered to be an independent risk factor for TTP. To resolve this apparent contradiction, we show that ADAMTS13 does not directly promote development of adipose tissue in a mouse model.