Fat cell function and fibrinolysis.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanisms linking adipose tissue function and PAI-1 regulation.
PubMed 11246816 · doi:10.1055/s-2007-978677
What was done
Narrative review evaluating the mechanistic links between adipose tissue function, insulin resistance, and circulating levels of plasminogen activator inhibitor-1 (PAI-1). The review discusses the contribution of visceral fat depots, cellular sources within adipose tissue, and regulatory factors including cytokines, free fatty acids, and hormones.
What was found
The abstract provides no numerical data or effect estimates. It notes that PAI-1 is elevated in insulin-resistant and obese states, with visceral adipose tissue—specifically stromal cells—serving as a key site of synthesis. Regulatory mediators discussed include TNF-alpha, TGF-beta, free fatty acids, insulin, and glucocorticoids.
Why it matters
It characterizes visceral adipose tissue as an active secretory source of prothrombotic factors like PAI-1, connecting metabolic disturbances directly to impaired fibrinolysis.
Limits
The publication is a narrative review with no primary patient data, sample sizes, or systematic study selection. The abstract does not report quantitative effect sizes or controlled clinical outcomes.
Cited by
- contradicts Adipose tissue is the primary source of plasminogen activator inhibitor-1 (PAI-1) in the body.