红细胞变形能力（red blood cell deformability，RCD）降低是糖尿病微血管病变的重要发病基础。以往研究主要集中于血红蛋白、膜蛋白及膜骨架非酶糖基化导致的细胞内液粘度增高及膜流动性和变形能力下降。然而，RCD与细胞内ATP水平密切相关，前期预实验发现高糖降低储存期RBC内ATP水平，且糖尿病微血管病变患者RBC内己糖激酶（hexokinase，HK）活性下降。由于糖尿病患者体内蛋白糖基化修饰非常普遍，因此推测高糖可能通过糖基化修饰HK影响RBC能量代谢进而降低RCD。本研究首先通过血流变、代谢组、细胞能量代谢分析及糖基化检测等明确高糖对体外培养RBC变形能力、糖酵解通量和中间产物以及HK活性和糖基化的影响，然后进一步分析微血管病变患者RBC内HK糖基化修饰与RCD的相关性，阐明微血管病变RCD下降的分子机制，为微血管病变的诊断、治疗和预防提供新的思路。

The decreased red blood cell deformability (RCD) is an important pathogenetic basis of diabetic microangiopathy. Previous studies mainly focused on the increase in intracellular fluid viscosity and the decrease in membrane fluidity and deformability, which were caused by non-enzymatic glycosylation of hemoglobin, membrane proteins, and membrane skeleton. However, RCD is also closely related to intracellular ATP levels. Pilot experimental results showed that high glucose can reduce the ATP levels in RBCs during storage, and the activity of hexokinase (HK), the first key enzyme of glycolysis, decreases in diabetic microangiopathy patients’ RBCs. Since protein glycosylation modification is very common in diabetic patients, we hypothesize that high glucose might reduce RCD though glycosylation of HK, which could further inhibit the RBC energy metabolism. This study aims to determine the deformability, glycolytic flux，intermediate metabolic products, as well as HK activity and glycosylation modification on high-glucose cultured RBCs firstly by hemorheological, metabolomic, Seahorse XF extracellular flux and glycosylation analyses. Then, the correlation between HK glycosylation and RCD in diabetic microangiopathy patients will be analyzed to further elucidate the molecular mechanisms of decreased RCD in diabetic microangiopathy patients, which will provide new ideas for the diagnosis, treatment and prevention of diabetic microangioathy patients.