Pathogenesis of feline diabetes mellitus
The insulin deficiency that occurs with diabetes impairs the uptake of glucose by cells, resulting in a great paradox: simultaneous extracellular hyperglycemia (elevated blood glucose) and intracellular glucose deficiency.
To compensate for the glucose deficiency, gluconeogenesis occurs. Because this process results in use of amino acids to produce glucose, there is a decrease in protein synthesis and subsequent weight loss and increased risk of infections resulting from antibody loss.
Excess glucose produced accumulates in the blood causing hyperglycemia. Small glucose molecules are freely filtered through the glomerulus in the kidney. In normal cats, the renal tubules will reabsorb the filtered glucose. However, if the blood glucose rises above the renal threshold of approximately 200 to 280 mg/dL in cats, these tubular reabsorption mechanisms are overwhelmed and glucose appears in the urine.
Glucose exerts an osmotic diuretic effect that leads to polyuria. To compensate, the cat experiences excessive thirst and polydipsia. Furthermore, the concentration of glucose in the bloodstream exerts an osmotic pressure and pulls fluid out of cells, resulting in cell dehydration. Without medical intervention, hyperglycemic coma and death can occur.
Figures 1 and 2 illustrate the consequences of the deadly paradox caused by diabetes: