Recently, while reviewing physiology, I found an answer to a question that had puzzled me for a long time: Internal medicine only explains that diabetes can cause various complications, damaging blood vessels, nerves, etc., leading to nephritis, arteriosclerosis, and so on. But why do these complications occur? How exactly are the blood vessels and nerves damaged?
Cells are just soaking in sugary water—at worst, a bit of dehydration.
Recently, reviewing physiology has somewhat answered this question. These mechanisms are probably very complex, so I will learn and supplement as I go. Discussion is welcome 
Analysis from Glucose Receptors
Cells need glucose receptors (GLUT) to absorb glucose. There are many subtypes of glucose receptors, with different distributions and properties.
The glucose receptor in the liver is GLUT4, which requires insulin to activate and absorb glucose to convert it into glycogen. In diabetes, glucose absorption by the liver is abnormal, causing persistent high blood sugar.
The glucose receptor in the lens (crystalline lens) does not require insulin to work, so when blood sugar is too high, it absorbs too much glucose. The proteins in the lens combine with glucose and denature, causing lens clouding.
Similarly, if a tissue has this type of insulin-independent GLUT, when blood sugar is high, it absorbs more glucose, triggering certain biochemical reactions, and that tissue essentially gets damaged.