So, now that we know Felicia has diabetes, we’ll briefly discuss the physiology behind her laboratory changes and her clinical signs.
Hyperglycemia: Initially, most cats have type-2 or non-insulin dependent diabetes mellitus. This means that their beta cells may not be producing an appropriate amount of insulin or they have some degree of insulin resistance or both. (This bit of feline physiology is what makes treating diabetic cats interesting.) Without insulin, glucose is unable to enter cells. Cellular starvation prompts catabolic processes which result in muscle wasting and weightloss. In the hypothalamus, glucose is unable to enter the satiety center cells so the feeling of hunger is uninhibited, resulting in polyphagia.
Glycosuria: The renal threshold for tubular reabsorption of glucose in cats is about 200 to 280 mg/dl. Above this amount, we start to see glucose in the urine. Fasting hyperglycemia and glycosuria are the hallmarks of diabetes mellitus.
Hyponatremia and hyperkalemia: Glucose spilling into the urine shifts the osmotic gradient. Hyperosmolar urine draws sodium and water out of the renal tubules, resulting in polyuria with a compensatory polydipsia.
