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Human visceral adipose tissue and the plasminogen activator inhibitor type 1.
Int J Obes (Lond) 2007; 31(11):1671-9IJ

Abstract

OBJECTIVE

The objective of this study was to systematically evaluate the molecular basis of the association between visceral fat mass and plasma plasminogen activator inhibitor-1 (PAI-1) levels in man.

DESIGN

A comprehensive approach comprising observational, in vitro, and human intervention studies.

MEASUREMENTS AND RESULTS

We confirmed an exclusive relationship between visceral fat and plasma PAI-1 levels (r=0.79, P<0.001) and corroborated preferential PAI-1 release from adipose tissue explants. Yet, messenger RNA analysis and in vivo measurement of PAI-1 release from visceral fat (AV-differences over the omentum) not only excluded visceral adipose tissue as a relevant source of circulating PAI-1, but also excluded visceral fat as a significant source of proinflammatory mediators such as tumor necrosis factor-alpha, IL-1 or transforming growth factor-beta that could induce PAI-1 expression in tissues other than visceral fat. Short-term interventions with acipimox and growth hormone (GH) as well as statistical evaluation excluded free fatty acids and GH as metabolic links. Further analysis of the metabolic data in a stepwise regression model indicated that plasma PAI-1 levels and visceral fat rather are co-correlates that both relate to impaired lipid handling.

CONCLUSION

Our PAI-1 studies show that visceral fat mass and plasma PAI-1 levels are co-correlated rather than causatively related, with lipid load as common denominator.

Authors+Show Affiliations

Department of Vascular Surgery, Leiden University Medical Center, Leiden, The Netherlands. Lindeman@lumc.nlNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17471294

Citation

Lindeman, J H N., et al. "Human Visceral Adipose Tissue and the Plasminogen Activator Inhibitor Type 1." International Journal of Obesity (2005), vol. 31, no. 11, 2007, pp. 1671-9.
Lindeman JH, Pijl H, Toet K, et al. Human visceral adipose tissue and the plasminogen activator inhibitor type 1. Int J Obes (Lond). 2007;31(11):1671-9.
Lindeman, J. H., Pijl, H., Toet, K., Eilers, P. H., van Ramshorst, B., Buijs, M. M., ... Kooistra, T. (2007). Human visceral adipose tissue and the plasminogen activator inhibitor type 1. International Journal of Obesity (2005), 31(11), pp. 1671-9.
Lindeman JH, et al. Human Visceral Adipose Tissue and the Plasminogen Activator Inhibitor Type 1. Int J Obes (Lond). 2007;31(11):1671-9. PubMed PMID: 17471294.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Human visceral adipose tissue and the plasminogen activator inhibitor type 1. AU - Lindeman,J H N, AU - Pijl,H, AU - Toet,K, AU - Eilers,P H C, AU - van Ramshorst,B, AU - Buijs,M M, AU - van Bockel,J H, AU - Kooistra,T, Y1 - 2007/05/01/ PY - 2007/5/2/pubmed PY - 2008/4/15/medline PY - 2007/5/2/entrez SP - 1671 EP - 9 JF - International journal of obesity (2005) JO - Int J Obes (Lond) VL - 31 IS - 11 N2 - OBJECTIVE: The objective of this study was to systematically evaluate the molecular basis of the association between visceral fat mass and plasma plasminogen activator inhibitor-1 (PAI-1) levels in man. DESIGN: A comprehensive approach comprising observational, in vitro, and human intervention studies. MEASUREMENTS AND RESULTS: We confirmed an exclusive relationship between visceral fat and plasma PAI-1 levels (r=0.79, P<0.001) and corroborated preferential PAI-1 release from adipose tissue explants. Yet, messenger RNA analysis and in vivo measurement of PAI-1 release from visceral fat (AV-differences over the omentum) not only excluded visceral adipose tissue as a relevant source of circulating PAI-1, but also excluded visceral fat as a significant source of proinflammatory mediators such as tumor necrosis factor-alpha, IL-1 or transforming growth factor-beta that could induce PAI-1 expression in tissues other than visceral fat. Short-term interventions with acipimox and growth hormone (GH) as well as statistical evaluation excluded free fatty acids and GH as metabolic links. Further analysis of the metabolic data in a stepwise regression model indicated that plasma PAI-1 levels and visceral fat rather are co-correlates that both relate to impaired lipid handling. CONCLUSION: Our PAI-1 studies show that visceral fat mass and plasma PAI-1 levels are co-correlated rather than causatively related, with lipid load as common denominator. SN - 0307-0565 UR - https://www.unboundmedicine.com/medline/citation/17471294/Human_visceral_adipose_tissue_and_the_plasminogen_activator_inhibitor_type_1_ L2 - http://dx.doi.org/10.1038/sj.ijo.0803650 DB - PRIME DP - Unbound Medicine ER -