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MIF deficiency does not alter glucose homeostasis or adipose tissue inflammatory cell infiltrates during diet-induced

Sarah J Conine1, Janet V Cross

  • 1Department of Pathology, The University of Virginia, Charlottesville, Virginia, USA.

Obesity (Silver Spring, Md.)
|June 28, 2013
PubMed
Abstract

Insights

Macrophage migration inhibitory factor (MIF) deficiency did not impact weight gain, glucose intolerance, or adipose tissue inflammation in mice fed a high-fat diet. The absence of MIF showed no effect on obesity development or metabolic responses.

Area of Science:

  • Immunology
  • Metabolic Research
  • Obesity Studies

Background:

  • Circulating macrophage migration inhibitory factor (MIF) levels correlate with body mass index (BMI) in humans.
  • MIF plays a role in immune responses and inflammation.
  • High-fat diet (HFD) is a common model for inducing obesity and metabolic dysfunction.

Purpose of the Study:

  • To investigate the role of MIF in high-fat diet-induced obesity.
  • To determine the effects of MIF deficiency on weight gain, metabolic responses, and adipose tissue inflammation.

Main Methods:

  • Mice with and without MIF (MIF WT and MIF(-/-)) were fed a high-fat diet for 15 weeks.
  • Weight, metabolic parameters (glucose tolerance, insulin levels), and immune cell infiltrates in adipose tissue were assessed.
  • Flow cytometry was used to analyze immune cell populations.

Main Results:

  • MIF deficiency did not alter weight gain or adipose tissue mass compared to wild-type mice on a HFD.
  • Both groups exhibited similar glucose intolerance and elevated fasted blood insulin levels.
  • No significant differences in myeloid-derived suppressor cells (MDSCs) or macrophage infiltration in adipose tissue were observed between MIF-deficient and wild-type mice.

Conclusions:

  • MIF deficiency does not influence the development of obesity or associated metabolic disturbances in mice fed a high-fat diet.
  • The study indicates that MIF is not a critical factor in HFD-induced obesity, glucose homeostasis, or adipose tissue inflammation.

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