Diabetes Mellitus

• The pancreas has endocrine and exocrine functions.
• The pancreatic acinar cells are responsible for the formation and secretion of digestive enzymes.
• The endocrine cells within the islets of Langerhans are responsible for glucose hemostasis. This is mainly achieved through the hormones glucagon and insulin.
• Glucagon is secreted from alpha cells and increases blood glucose levels by converting stored glycogen in the lover into glucose.
• Insulin is released from beta cells in response to elevated blood glucose levels. This hormone reduces blood glucose by stimulating fat, liver, and muscle tissue to store glucose, reducing circulating glucose levels.
• Glucagon and insulin are released as required based on the body's blood glucose level, and counteract each other to maintain normoglycaemia in a healthy patient.
• In a diabetic patient, this balance of hormones is disrupted and blood glucose levels rise.
• In 80 to 90 percent of cats, diabetes is caused by a combination of insulin resistance and beta cell failure. This is more like human type two diabetes.
• Insulin resistance is the reduced efficacy of insulin action in the liver, adipose, and muscle tissue.
• 10 to 20 percent of cats have more specific causes of diabetes mellitus. These include acromegaly, hyperadrenocorticism, pancreatitis, and pancreatic lesions.
• Acromegaly is where a benign pituitary gland mass causes excessive release of growth hormone, which causes insulin resistant diabetes.
• Hyperadrenocorticism is also known as Cushing's disease.
• As diabetic cats have insulin resistance and beta cell failure, as opposed to absolute insulin deficiency, they can achieve remission if their disease is identified early and tightly controlled from an early stage.
• The pathophysiology of diabetes mellitus in cats differs significantly from dogs, the majority of whom have an absolute insulin deficiency due to immune mediated destruction of the beta cells. This is akin to type 1 diabetes in humans.
• Diabetes mellitus in dogs results in the absolute deficiency of insulin, meaning they will require lifelong treatment with no ability to enter diabetic remission.
• Other causes of canine diabetes mellitus include pregnancy or gestational diabetes, the use of certain medications, and hyperadrenocorticism.
• 5 percent of Cushingoid dogs are reportedly also diabetic, compared with 80 percent of Cushingoid cats.
• Diabetes risk factor for cats are obesity (causing insulin resistance), increasing age, indoor only access, physical inactivity, male gender, neutering, Burmese cats, and the administration of steroids and progestogens.
• Diabetes risks for dogs are middle to older age (or 7 plus), female, and breeds like Schnauzers, Siberian Huskies, Finnish Spitzes, Samoyeds, Golden Retrievers, and some terriers.
• Signs of feline diabetes are polyuria, weight loss, polydipsia, weakness, decreased appetite, fatigue, dehydration, and vomiting.
• Hyperglycemia in diabetic patients leads to glucose toxicity, which causes further damage to beta cells, decreasing insulin secretion and increasing insulin resistance even further.
• The cycle of glucose toxicity is hyperglycemia, then glucose toxicity, then insulin resistance and decreased secretion, then hyperglycemia. The continuation of this cycle can cause irreversible pancreatic damage, preventing the opportunity to achieve remission in cats.
• When glucose levels exceed the renal threshold, glucose spills from the bloodstream into the urine. This is the point where clinical signs of diabetes mellitus are usually seen.
• The renal threshold in dogs is 10 to 12 mmol/L
• The renal threshold in cats in 14 to 16 mmol/L.
• The classic signs of diabetes mellitus are polyuria, polydipsia, polyphagia, and weight loss.
• If diabetes remains undiagnosed for some time, ketone bodies are formed from lipids as an alternative energy source in the process of diabetic ketoacidosis.
• Diabetic ketoacidosis results in metabolic acidosis and ketosis.
• Signs for diabetic ketoacidosis are vomiting, anorexia, weight loss, dull mentation and dehydration.
• Patients with diabetic ketoacidosis require prompt stabilization and intensive nursing care prior to long term diabetic management.
• When investigating a potential case of diabetes mellitus, a number of diagnostic tests may be performed. There typically include a full biochemistry, electrolytes, hematology, and urinalysis, alongside other specific tests.
• Parameters of importance when testing for diabetes are glucose, fructosamine, biochemistry, total +/- free T4, pancreatic lipase (PLi), and urinalysis.
• A urine culture should always be performed since diabetic patients are at increased risk of urinary tract infection due to glucosuria +/- dilute urine.
• A cystocentesis sample should always be obtained for culture in order to avoid external contamination.
• The main goals of diabetic treatment are to resolve the patient's clinical signs while avoiding hypoglycemia.
• Resolution of clinical signs is achieved by maintaining the patient's blood glucose levels below the renal threshold as much as possible or below 11 mmol/L to prevent further glucose toxicity.
• Ideally diabetic patients should return to a normal appetite and water intake, and maintain a stable bodyweight.
• In cats, reverting the patient back to a subclinical state, achieving diabetic remission should be a treatment goal, though it may not be possible if the patient has been hyperglycemic for some time.
• Treatment usually consists of exogenous insulin administration, dietary modifications, weight loss in overweight patients, management of any concurrent diseases, and withdraw of any dibetogenic medications, like steroids.
• Administration of insulin is the main component of treatment in diabetic patients. Many different insulin types are available for use (neutral, protamine zinc, and glargine). Each have different durations and action and nadirs, both in dogs and cats.