symptoms of feline diabetes

Patients with this most common form of diabetes have an insensitivity to endogenous insulin. When an associated defect of insulin production prevents adequate compensation for this insulin resistance, nonketotic mild diabetes occurs. Hyperplasia of pancreatic B cells is often present and probably accounts for the fasting hyperinsulinism and exaggerated insulin and proinsulin responses to glucose and other stimuli seen early in the disease. After several years' duration of diabetes, chronic deposition of amyloid in the islets may combine with inherited genetic defects to progressively impair B cell function.
The mechanisms underlying the insulin resistance of type 2 diabetes are poorly understood. Obesity is generally associated with abdominal distribution of fat, producing an abnormally high waist-to-hip ratio. This "visceral" obesity, due to accumulation of fat in the omental and mesenteric regions, correlates with insulin resistance; subcutaneous abdominal fat seems to have less of an association with insulin insensitivity. Exercise may affect the deposition of visceral fat as suggested by CT scans of Japanese wrestlers, whose extreme obesity is predominantly subcutaneous. Their daily vigorous exercise program prevents accumulation of visceral fat, and they have normal serum lipids and euglycemia despite daily intakes of 5000-7000 kcal and development of massive subcutaneous obesity. Several adipokines, secreted by fat cells, can affect insulin action in obesity. Two of these, leptin and adiponectin, seem to increase sensitivity to insulin, presumably by increasing hepatic responsiveness. Two others — tumor necrosis factor-a, which inactivates insulin receptors, and the newly discovered peptide resistin — interfere with insulin action on glucose metabolism and have been reported to be elevated in obese animal models. Mutations or abnormal levels of these adipokines may contribute to the development of insulin resistance in human obesity.
Hyperglycemia per se can impair insulin action by causing accumulation of hexosamines in muscle and fat tissue and inhibiting glucose transport (acquired glucose toxicity). Correction of hyperglycemia reverses this acquired insulin resistance.