MiR-130b promotes obesity associated adipose tissue inflammation and insulin resistance in diabetes mice through alleviating M2 macrophage polarization via repression of PPAR-γ.

Inflammatory pathways play an important role in impaired glucose metabolism and insulin production. Adipose tissue inflammation is characterized by infiltration and expansion of macrophages, leading to type 2 diabetes (T2D). Macrophage polarization contributes to various inflammatory responses and cytokine production profiles. MiR-130b is involved in regulating immune response and metabolism. However, the specific role in macrophage polarization and glucose metabolism of T2D has not been reported. In this study, C57BL/6 mice were fed a high-fat diet to induce T2D mice model. The peritoneal macrophages were isolated, miR-130b and M1/M2 polarization was analyzed. Glucose tolerance was also detected. In addition, the relationship between miR-130b and the target gene was identified. We showed that mice fed on high-fat diet demonstrated significantly higher body weight and impaired glucose tolerance. In addition, the miR-130b level was up-regulated in macrophage of high-fat diet mice, which regulated M1/M2 polarization, adipose tissue inflammation and glucose tolerance. Furthermore, we identified PPAR-γ as a miR-130b target gene and regulated macrophage polarization. In summary, our findings demonstrated that miR-130b was a novel regulator of macrophage polarization and contributed to adipose tissue inflammation and insulin tolerance via repression of PPAR-γ. Furthermore, miR-130b represented a promising target for T2D therapy in the clinic.