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

While HFD feeding induced obesity with the expected perturbations in glucose homeostasis and adipose tissue inflammation, the presence or absence of MIF had no effect on any parameter examined.

MIF wild type (MIF WT) and MIF deficient (MIF(-/-)) C57Bl/6J mice were fed a high-fat diet (HFD) for up to 15 weeks. Weight and metabolic responses were measured over the course of the disease. Immune cell infiltrates in visceral and subcutaneous adipose tissue were examined by flow cytometry.

Circulating macrophage migration inhibitory factor (MIF) levels have been shown to positively correlate with body mass index (BMI) in humans. Our objective in this study was to determine the effects of MIF deficiency in a model of high-fat diet-induced obesity. Design and

There was no difference in weight gain or adipose tissue mass in MIF(-/-) mice compared to MIF WT mice. Both groups fed HFD developed glucose intolerance at the same rate and had similar elevations in fasted blood insulin. MDSC abundance was evaluated and showed no MIF-dependent differences. Macrophages were elevated in the visceral adipose tissue of obese mice, but there was no difference between the two groups. Conclusions: While HFD feeding induced obesity with the expected perturbations in glucose homeostasis and adipose tissue inflammation, the presence or absence of MIF had no effect on any parameter examined.