Pathophysiological roles of monocyte insulin signaling and NF-kBactivation in diabetes

在这项研究中，我们研究了单核/巨噬细胞炎症和增殖在糖尿病进展中的意义。高糖条件下培养的巨噬细胞和单核细胞表现出明显的炎症活性，高糖搏动刺激可显著增加炎症细胞因子的表达。随着炎症活性的增加，细胞周期抑制因子p27kip的表达增加，巨噬细胞的增殖受到抑制。另一方面，巨噬细胞特异性p27kip转基因小鼠的巨噬细胞增殖受到抑制，在高脂饮食负荷后表现出改善的糖耐量。需要进一步的研究来揭示单核/巨噬细胞炎症和增殖在糖尿病进展中的病理生理作用。

In this study we investigate the implication of monocyte/macrophage inflammation andproliferation in diabetes progression. Macrophage and monocyte cultured in high glucoseshowed activated inflammatory activity, and pulsate stimulation with high glucose inducedsignificantly increased inflammatory cytokine expression. Along with the increase ofinflammatory activity, the cell cycle inhibitor, p27kip expression was increased, andmacrophage proliferation was inhibited in high glucose culture. On the other hand, themacrophage specific p27kip transgenic mouse, whose macrophage proliferation is inhibited,showed improved glucose tolerance after high fat diet loading. Further studies arenecessary to reveal the pathophysiological roles of monocyte/macrophage inflammation andproliferation in the progression of diabetes.