Figure 5.

Excess acetyl-CoA drives nonenzymatic protein acetylation. For noninsulin-dependent cells, diabetic hyperglycemia can overload them with glucose, causing the oversupply of acetyl-CoA. For insulin-dependent tissues in diabetes, the cell cannot get enough glucose and will have to use fatty acids as the source of energy. Because oxaloacetate cannot be continuously formed due to lack of glucose, the level of acetyl-CoA could be extremely high, leading to ketone body production and protein acetylation.