Irisin ameliorates obesity and insulin resistance via adipose tissue IL-33 and regulatory T cells.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Irisin is an exercise-induced myokine that confers multiple physiological benefits, including browning of subcutaneous adipose tissue in mice. However, the underlying cellular and molecular mechanisms of irisin's effects on obesity are unclear. Here, we show that irisin modulates adipose tissue inflammation by increasing interleukin (IL)-33 production and preserving ST2 + regulatory T cells in white adipose tissues. Administered chronically to high-fat-diet-fed male mice, irisin preserves visceral adipose tissue (VAT) levels of ST2 + regulatory T cells, an important immunomodulatory population that usually contracts after long-term high-fat-diet feeding. This protection results from increases in IL-33-producing mesenchymal stromal cells and IL-33 levels in VAT. These effects are primary, as irisin directly induces IL-33 expression in cultured VAT mesenchymal stromal cells. Irisin-mediated changes in VAT IL-33 dynamics are accompanied by IL-33-dependent upregulation of thermogenic gene expression in subcutaneous adipose tissue. These irisin-driven cell-cell and inter-tissue interactions improve obesity and glucose intolerance, and increase energy expenditure, with no reduced food intake and muscle loss in obese mice.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.