Recombinant Macrophage Migration Inhibitory Factor Derived from Trichinella spiralis Suppresses Obesity by Reducing Body Fat and Inflammation

TL;DR

A recombinant protein from a parasitic worm reduces obesity in mice by lowering body fat and inflammation.

Contribution

A novel recombinant protein from Trichinella spiralis shows anti-obesity and anti-inflammatory effects in mice.

Findings

Oral rTs-MIF reduced body weight, fat mass, and glucose levels in high-fat diet-fed mice.

rTs-MIF decreased pro-inflammatory cytokines and increased M2 macrophage markers.

In cells, rTs-MIF inhibited fat cell formation and modulated key signaling pathways.

Abstract

Obesity, an escalating global health crisis, is characterized by adipose tissue hypertrophy and chronic low-grade inflammation. Although anti-obesity drugs can induce weight loss, their use is limited by adverse effects, underscoring the need for safer therapeutic strategies. In this study, we generated a recombinant form of Trichinella spiralis-derived macrophage migration inhibitory factor (rTs-MIF) and investigated its anti-inflammatory and anti-obesity effects via immunometabolic regulation. Male C57BL/6 mice fed a 45% high-fat diet were orally administered rTs-MIF, and its effects were evaluated by measuring fat mass, glucose metabolism, serum cytokines, liver histology, and adipose tissue parameters. In 3T3-L1 cells, we examined the effects of rTs-MIF on adipocyte differentiation, obesity-related gene expression, and intracellular signaling pathways. Oral rTs-MIF suppressed body weight gain, reduced fat mass, improved glucose levels, and decreased the food efficiency ratio. It also lowered pro-inflammatory cytokines and increased markers associated with M2 macrophages. In 3T3-L1 cells, rTs-MIF inhibited adipocyte differentiation and reduced the expression of lipogenic transcription factors and mouse Mif while modulating AKT and p44/42 MAPK signaling. These findings identify rTs-MIF as a potential bioactive candidate that ameliorates obesity by regulating the immune–metabolic axis.

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