Coagulation and fibrinolysis abnormalities in obesity
Abstract
Abnormalities in coagulation and haemostasis represent a well-known link between obesity and thrombosis (both arterial and venous). Several studies have shown that obese patients have higher plasma concentrations of all pro-thrombotic factors (fibrinogen, vonWillebrand factor (vWF), and factor VII), as compared to non-obese controls, with a positive association with central fat. Similarly, plasma concentrations of plasminogen activator inhibitor-1 (PAI-1) have been shown to be higher in obese patients as compared to non-obese controls and to be directly correlated with visceral fat. Furthermore, obesity is characterized by higher plasma concentrations of anti-thrombotic factors, such as tissue-type plasminogen activator (t-PA) and protein C, as compared to non-obese controls, the increase in these factors being likely to represent a protective response partly counteracting the increase in pro-thrombotic factors. The issue of whether adipose tissue contributes directly to plasma PAI-1, its products stimulating other cells to produce PAI-1, or whether it primarily contributes indirectly has not yet been resolved. It has been proposed that the secretion of interleukin-6 (IL-6) by adipose tissue, combined with the actions of adipose tissue-expressed TNF-alpha in obesity, could underlie the association of insulin resistance with endothelial dysfunction, coagulopathy, and coronary heart disease. The role of leptin in impairing haemostasis and promoting thrombosis has been recently reported. Finally, some hormonal abnormalities (androgen, F, catecholamines) associated with the accumulation of body fat may contribute to the impairment of coagulative pathway in obesity. As to intervention strategies, dietary (i.e., low-fat high-fiber diet) and lifestyle (i.e., physical activity) measures have been demonstrated to be effective in improving the obesity-associated pro-thrombotic risk profile.
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The MS may increase cardiovascular event risk through prothrombotic or inflammatory mechanisms rather than by accelerating atherosclerotic progression.
“Whereas the MS may play a limited role in accelerating atherosclerotic progression, it may significantly increase the risk of vascular events through prothrombotic or inflammatory mechanisms.29 -31”
From Diabetes, the Metabolic Syndrome, and Angiographic Progression of Coronary Arterial Disease in Postmenopausal Women (2006) · cites this paper as [29]
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- Authors
- De Pergola, G., & Pannacciulli, N.
- Affiliations
- University of Bari Aldo Moro (IT)
- Venue
- Journal of Endocrinological Investigation
- Published
- 2002-11
- Volume
- 25
- Issue
- 10
- Pages
- 899-904
- ISSN
- 0391-4097 (ISSN-L)
- 1720-8386
- OpenAlex
- W2033958201
- Cited by
- 206
- References
- 39
- Citations by year
- 2026: 8 · 2025: 4 · 2024: 7 · 2023: 6 · 2022: 13 · 2021: 9 · 2020: 9 · 2019: 7 · 2018: 8 · 2017: 3 · 2016: 8 · 2015: 7 · 2014: 9 · 2013: 6 · 2012: 8
- FWCI
- 1.45
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Journal of Endocrinological Investigation (publishedVersion)
- PubMed (publishedVersion)
- CINECA IRIS Institutional Research Information System (University of Bari Aldo Moro) (submittedVersion)
- Topics
- Health Sciences › Medicine › Hematology › Blood Coagulation and Thrombosis Mechanisms
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Blood properties and coagulation
- Keywords
- obesity, coagulopathy, fibrinolysis, thrombosis, hemostasis, plasminogen activator inhibitor-1, tissue plasminogen activator, protein C, fibrinogen, von Willebrand factor, factor VII, visceral fat, adipose tissue, interleukin-6, TNF-α, insulin resistance, endothelial dysfunction, coronary artery disease, leptin, androgens, catecholamines, low-fat high-fiber diet, physical activity
- MeSH terms
- Adipose Tissue, Blood Coagulation Disorders, Endocrine Glands, Fibrinolysis, Hemostasis, Humans, Insulin Resistance, Obesity, Polymorphism, Genetic, Thrombosis, Plasminogen Activator Inhibitor 1, Leptin
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