Paper

International Journal of Obesity (2005) 29, 675–681. doi:10.1038/sj.ijo.0802942 Published online 29 March 2005

Obesity, macrophage migration inhibitory factor, and weight loss

T S Church1, M S Willis2, E L Priest1, M J LaMonte1, C P Earnest1, W J Wilkinson1, D A Wilson3 and B P Giroir3

  1. 1The Cooper Institute, 12330 Preston Road, Dallas, TX, USA
  2. 2Department of Pathology, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX, USA
  3. 3Department of Pediatrics, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX, USA

Correspondence: Dr TS Church, Centers for Integrated Health Research, The Cooper Institute, 12330 Preston Road, Dallas, TX 75230, USA. E-mail: tchurch@cooperinst.org

Received 19 August 2004; Accepted 13 December 2004; Published online 29 March 2005.

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Abstract

OBJECTIVE:

 

Elevated macrophage migration inhibitory factor (MIF) has been implicated as a causal mechanism in a number of disease conditions including cardiovascular disease (CVD), diabetes, and cancer. Excess body fat is associated with an increased risk of numerous health conditions including CVD, diabetes, and cancer. To our knowledge, the association between MIF and obesity status and the effect of weight loss on serum MIF concentrations have not been reported. In this study, we examined the effects of participation in a behavior-based weight loss program on MIF concentrations in obese individuals.

SUBJECTS:

 

Study participants were 71 men and women enrolled in The Cooper Institute Weight Management Program. Participants were predominantly female (68%, n=48), middle-aged (46.5plusminus9.8 y), and severely obese (BMI=43.0plusminus8.6).

METHOD:

 

Plasma MIF concentrations and other standard risk factors were measured before and after participation in a diet and physical activity based weight management program.

RESULTS:

 

The mean follow-up was 8.5plusminus3.0 months with an average weight loss of 14.4 kg (P<0.001). The majority of clinical risk factors significantly improved at follow-up. Median levels of plasma MIF concentration were significantly lower at follow-up (median [IQR]; 5.1[3.6–10.3]) compared to baseline (8.4 [4.3–48.8]; P=0.0005). The percentage of participants with plasma MIF concentration greater than or equal to19.5 mg/nl (highest tertile at baseline) decreased from 33.8 to 5.6% (P<0.001). Further, elevated baseline plasma MIF concentration was associated with markers of beta-cell dysfunction and reductions in MIF were associated with improvements in beta-cell function.

CONCLUSIONS:

 

Circulating MIF concentrations are elevated in obese but otherwise healthy individuals; however, this elevation in MIF is not uniform across individuals. In obese individuals with elevated circulating MIF concentrations, participation in physical activity and a dietary-focused weight management program resulted in substantial reduction in MIF.

Keywords:

cytokines, MIF, HOMA, intervention

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