| First Author | De Taeye BM | Year | 2006 |
| Journal | J Biol Chem | Volume | 281 |
| Issue | 43 | Pages | 32796-805 |
| PubMed ID | 16931518 | Mgi Jnum | J:117279 |
| Mgi Id | MGI:3695952 | Doi | 10.1074/jbc.M606214200 |
| Citation | De Taeye BM, et al. (2006) Bone marrow plasminogen activator inhibitor-1 influences the development of obesity. J Biol Chem 281(43):32796-805 |
| abstractText | Plasma levels of plasminogen activator inhibitor-1 (PAI-1) are elevated in obesity and correlate with body mass index. The increase in PAI-1 associated with obesity likely contributes to increased cardiovascular risk and may predict the development of type 2 diabetes mellitus. Although adipocytes are capable of synthesizing PAI-1, the bulk of evidence indicates that cells residing in the stromal fraction of visceral fat are the primary source of PAI-1. We hypothesized that bone marrow-derived PAI-1, e.g. derived from macrophages located in visceral fat, contributes to the development of diet-induced obesity. To test this hypothesis, male C57BL/6 wild-type mice and C57BL/6 PAI-1 deficient mice were transplanted with either PAI-1(-/-), PAI-1(+/-), or PAI-1(+/+) bone marrow. The transplanted animals were subsequently fed a high fat diet for 24 weeks. Our findings show that only the complete absence of PAI-1 protects from the development of diet-induced obesity, whereas the absence of bone marrow-derived PAI-1 protects against expansion of the visceral fat mass. Remarkably, there is a link between the PAI-1 levels, the degree of inflammation in adipose tissue, and the development of obesity. Based on these findings we suggest that bone marrow-derived PAI-1 has an effect on the development of obesity through its effect on inflammation. |
