Tags

Type your tag names separated by a space and hit enter

Obesity and impaired fibrinolysis: role of adipose production of plasminogen activator inhibitor-1.
Int J Obes Relat Metab Disord 2004; 28(11):1357-64IJ

Abstract

Obesity is the central promoter of the metabolic syndrome which also includes disturbed fibrinolysis in addition to hypertension, dyslipidaemia and impaired glucose tolerance/type 2 diabetes mellitus. Plasminogen activator inhibitor-1 (PAI-1) is the most important endogenous inhibitor of tissue plasminogen activator and uro-plasminogen activator, and is a main determinant of fibrinolytic activity. There is now compelling evidence that obesity and, in particular, an abdominal type of body fat distribution are associated with elevated PAI-1 antigen and activity levels. Recent studies established that PAI-1 is expressed in adipose tissue. The greater the fat cell size and the adipose tissue mass, the greater is the contribution of adipose production to circulating PAI-1. Experimental data show that visceral adipose tissue has a higher capacity to produce PAI-1 than subcutaneous adipose tissue. Studies in human adipocytes indicate that PAI-1 synthesis is upregulated by insulin, glucocorticoids, angiotensin II, some fatty acids and, most potently, by cytokines such as tumour necrosis factor-alpha and transforming growth factor-beta, whereas catecholamines reduce PAI-1 production. Interestingly, pharmacological agents such as thiazolidinediones, metformin and AT(1)-receptor antagonists were found to reduce adipose expression of PAI-1. In addition, weight loss by dietary restriction or comprehensive lifestyle modification is effective in lowering PAI-1 plasma levels. In conclusion, impaired fibrinolysis in obesity is probably also due to an increased expression of PAI-1 in adipose tissue. An altered function of the endocrine system and an impaired auto-/paracrine function at the fat cell levels may mediate this disturbance of the fibrinolytic system and thereby increase the risk for cardiovascular disease..

Authors+Show Affiliations

Else Kröner-Fresenius-Centre for Nutritional Medicine, Technical University of Munich, Freising-Weihenstephan, Germany.No affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

15356668

Citation

Skurk, T, and H Hauner. "Obesity and Impaired Fibrinolysis: Role of Adipose Production of Plasminogen Activator Inhibitor-1." International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity, vol. 28, no. 11, 2004, pp. 1357-64.
Skurk T, Hauner H. Obesity and impaired fibrinolysis: role of adipose production of plasminogen activator inhibitor-1. Int J Obes Relat Metab Disord. 2004;28(11):1357-64.
Skurk, T., & Hauner, H. (2004). Obesity and impaired fibrinolysis: role of adipose production of plasminogen activator inhibitor-1. International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity, 28(11), pp. 1357-64.
Skurk T, Hauner H. Obesity and Impaired Fibrinolysis: Role of Adipose Production of Plasminogen Activator Inhibitor-1. Int J Obes Relat Metab Disord. 2004;28(11):1357-64. PubMed PMID: 15356668.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Obesity and impaired fibrinolysis: role of adipose production of plasminogen activator inhibitor-1. AU - Skurk,T, AU - Hauner,H, PY - 2004/9/10/pubmed PY - 2004/12/29/medline PY - 2004/9/10/entrez SP - 1357 EP - 64 JF - International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity JO - Int. J. Obes. Relat. Metab. Disord. VL - 28 IS - 11 N2 - Obesity is the central promoter of the metabolic syndrome which also includes disturbed fibrinolysis in addition to hypertension, dyslipidaemia and impaired glucose tolerance/type 2 diabetes mellitus. Plasminogen activator inhibitor-1 (PAI-1) is the most important endogenous inhibitor of tissue plasminogen activator and uro-plasminogen activator, and is a main determinant of fibrinolytic activity. There is now compelling evidence that obesity and, in particular, an abdominal type of body fat distribution are associated with elevated PAI-1 antigen and activity levels. Recent studies established that PAI-1 is expressed in adipose tissue. The greater the fat cell size and the adipose tissue mass, the greater is the contribution of adipose production to circulating PAI-1. Experimental data show that visceral adipose tissue has a higher capacity to produce PAI-1 than subcutaneous adipose tissue. Studies in human adipocytes indicate that PAI-1 synthesis is upregulated by insulin, glucocorticoids, angiotensin II, some fatty acids and, most potently, by cytokines such as tumour necrosis factor-alpha and transforming growth factor-beta, whereas catecholamines reduce PAI-1 production. Interestingly, pharmacological agents such as thiazolidinediones, metformin and AT(1)-receptor antagonists were found to reduce adipose expression of PAI-1. In addition, weight loss by dietary restriction or comprehensive lifestyle modification is effective in lowering PAI-1 plasma levels. In conclusion, impaired fibrinolysis in obesity is probably also due to an increased expression of PAI-1 in adipose tissue. An altered function of the endocrine system and an impaired auto-/paracrine function at the fat cell levels may mediate this disturbance of the fibrinolytic system and thereby increase the risk for cardiovascular disease.. UR - https://www.unboundmedicine.com/medline/citation/15356668/Obesity_and_impaired_fibrinolysis:_role_of_adipose_production_of_plasminogen_activator_inhibitor_1_ L2 - http://ovidsp.ovid.com/ovidweb.cgi?T=JS&PAGE=linkout&SEARCH=15356668.ui DB - PRIME DP - Unbound Medicine ER -