Diabetes is one of the complex diseases characterised by grossly abnormal fuel usage: glucose is overproduced by the liver but underutilised by other organs.
In type 1 diabetes, insulin is absent and consequently glucagon is present at high amounts than normal physiologic levels. In essence, the daibetic person is in what is usually termed, biochemical starvation mode despite a high blood glucose concentration. One major function of insulin is to increase cells' sensitivity to glucose and increase their uptake (through GLUT receptors). Because insulin is absent, the entry of glucose into cells is impaired.
The liver then becomes stuck in gluconeogenic and ketogenic mode. The excess level of glucagon relative to insullin leads to decrease in the amount of F-2,6-BP in the liver, hence glycolysis is inhibited and gluconeogenesis is stimulated because of the complementary effects of F-2,6-BP on PFK and FBPase.
Because carbohydrate utilisation is impaired, a lack of insulin leads to the uncontrolled breakdown of lipids and proteins. However, breakdown of lipids generate more acteyl CoAs which cannot enter citric acid cycle (why?); instead, ketone bodies are produced.
This ecplains why Diabetic patients usually suffer a biochemical condition called, Diabetic Ketoacidosis. Coma is highly to occur simply because of the severely lowered blood PH (same effect that will happen if you were put in an enclosed place full of CO2).