Macrophage inhibitory factor, plasminogen activator inhibitor-1, other acute phase proteins, and inflammatory mediators normalize as a result of weight loss in morbidly obese subjects treated with gastric restrictive surgery

F. van Dielen*, W.A. Buurman, M. Hadfoune, J. Nijhuis, J.W. Greve

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Obesity is demonstrated to be associated with an enhanced inflammatory state, which is suggested to be a cause for the development of obesity-related morbidity. It was hypothesized that a decrease in body weight in morbid obese subjects would lead to a reduction of the inflammatory state in these subjects.Weight loss was achieved by gastric restrictive surgery in 27 morbidly obese patients. Preoperative as well as 3-, 6-, 12-, and 24-month postoperative plasma concentrations of inflammatory mediators macrophage inhibitory factor, plasminogen activator inhibitor-1, lipopolysaccharide binding protein, alpha-1 acid glycoprotein, C-reactive protein, soluble TNFalpha receptors 55 and 75, and leptin were measured.Macrophage inhibitory factor levels remained low normal for 6 months, during weight loss, after which they significantly increased to normal levels at 24 months postoperatively. The other inflammatory mediators remained elevated up to minimally 3 months postoperatively; thereafter they decreased significantly. Both TNFalpha receptors remained elevated up to at least 12 months postoperatively to decrease significantly at 2 yr postoperatively.This study demonstrates that during weight loss, after gastric restrictive surgery, inflammatory mediators remain elevated for at least 3 months postoperatively, suggesting initially an ongoing inflammatory state. However, 2 yr after surgery, the inflammatory mediators reach near normal values.These findings may be an explanation for the reduced comorbidity seen in morbidly obese patients after gastric restrictive surgery.
Original languageEnglish
Pages (from-to)4062-4068
JournalJournal of Clinical Endocrinology & Metabolism
Volume89
Issue number8
DOIs
Publication statusPublished - 1 Jan 2004

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