A cross-talk between diabetes and malaria within-host is well established. Diabetes is associated with modulation of the immune system, impairment of the healing process and to disturb the host metabolism to contribute towards propagation of parasite infection. Glucose metabolism in host is maintained by insulin and RBC has 2000 insulin receptor present on plasma membrane. These receptors are robust to relay down-stream signaling in RBCs but role of intracellular signaling in parasite growth is not been explored. The malaria parasite treated with insulin (100 ng/ml) is giving stimulation in parasite growth. The effect is lasting for several generations resulting into high parasitemia. Insulin signaling is phosphorylating protein in infected RBCs and level is high in parasite RBCs compared to uninfected RBCs. It is phosphorylating Spectrin-(α/β), Band-4.2, Ankyrin and the other proteins of RBC cytoskeleton. It in-turn induces enhanced glucose uptake inside infected RBCs. There is a high level of infection of normal RBCs by merozoites. In summary, insulin and glucose metabolism plays a crucial role in parasite propagation, disease severity and need consideration while treating patients.

宿主内糖尿病与疟疾之间的相互影响已得到很好的确立。糖尿病与免疫系统的调节，愈合过程的损害以及干扰宿主的新陈代谢有关，从而有助于寄生虫感染的传播。胰岛素维持宿主体内的葡萄糖代谢，并且红细胞在质膜上存在2000种胰岛素受体。这些受体对中继红细胞中的下游信号传导具有鲁棒性，但尚未探讨细胞内信号传导在寄生虫生长中的作用。胰岛素（100 ng / ml）处理过的疟原虫正在刺激寄生虫的生长。这种作用持续了几代，导致高寄生虫血症。与未感染的RBC相比，胰岛素信号传导使被感染的RBC中的蛋白质磷酸化，并且寄生虫RBC中的水平很高。它正在磷酸化血影蛋白-（α/β），Band-4.2，锚蛋白和RBC细胞骨架的其他蛋白质。反过来，它会在感染的RBC中诱导葡萄糖摄取的增加。裂殖子对正常红细胞的感染程度很高。总之，胰岛素和葡萄糖代谢在寄生虫繁殖，疾病严重程度中起着至关重要的作用，在治疗患者时需要考虑。