Our cats are susceptible to two varieties of feline diabetes. Diabetes insipidus is quite rare but can occur in any cat of any age. The far more common diabetes mellitus is similar to human diabetes mellitus type II. It is therefore most common in middle-aged to older cats, with an increased likelihood in overweight cats, particularly those that are excessively overweight or obese. It's thought that toms may be more prone to diabetes mellitus than queens.
Diabetes Insipidus
Central or hypophyseal diabetes insipidus (CDI) is due to the reduced manufacture of antidiuretic hormone (ADH) caused by damage to the hypothalamus, which is located below the brain. The damage may be caused by a neoplasm (cancer), cysts, an inflammatory granuloma (clump of monocyte or macrophage white blood cells) possibly resulting from an infection, or internal hemorrhaging (bleeding) resulting from a head trauma (injury).
Nephrogenic diabetes insipidus (NDI) results from the tubules (small tubes) in the kidneys failing to respond appropriately to normal and increasing levels of ADH in the blood. NDI may result from a blockage in the urinary tract, high calcium or low potassium levels in the blood, or from the use of some drugs, such as amphotericin B, which is an antifungal agent that is sometimes used to treat infections of yeast or fungi.
ADH is the hormone that controls the reabsorbtion of water by the kidneys during the blood filtering process that results in urine. If the cat's blood pressure is high, ADH production reduces so that more water is left in the urine, thus reducing blood volume and pressure. If it's low, more ADH is produced increasing the amount of water reabsorbed and at the same time the cat experiences thirst, so it will drink more and increase blood volume and thus pressure that way as well.
So the primary clinical sign for either type of diabetes insipidus is polyuria (increased urination) and this will occur whether the cat is drinking or not. The urine being produced will have a high water content, so will be quite pale, although getting to see this may be difficult. You might keep your cat enclosed in the bathroom with plenty of water until they are forced to urinate on the floor, thus letting you see the color. An injury to the hypothalamus may also short-circuit the thirst impulse, but if not or the cat has NDI it will also display polydipsia (an increased thirst). If the cat is not drinking, dehydration can occur very rapidly and quickly become life-threatening.
As stated earlier, this is a rare illness, but if your cat starts urinating more than normal, whether with increased thirst or not, you need to consult your veternarian. If this occurs within a few weeks of a head injury it would be best to take him or her into your veterinary clinic as soon as possible, to be on the safe side. Keep your cat well supplied with water while you are doing so.
Diabetes Mellitus
Diabetes mellitus is a chronic (develops over time) illness that causes problems in the metabolizing of carbohydrates due to a reduction in the production of the hormone insulin. Insulin is produced in the beta cells of the Islets of Langerhans in the pancreas in a continual process; the amount being produced is raised or lowered in response to, respectively, an increase or decrease in the concentration of glucose in the blood, often referred to as the blood sugar level.
Besides insulin, the beta cells also produce islet-associated polypeptide (IAPP) which cats have difficulty processing normally. This leads to a build-up over time of an excessive amount of IAPP which converts into amyloid, a hard, waxy, starchlike substance which damages the beta cells, a disease called amyloidosis. Destroyed islet cells are replaced by connective tissue unable to produce insulin. As more beta cells are damaged, the ability of the pancreas to manufacture insulin is reduced. When it is no longer able to produce sufficient insulin to meet the cat's needs, the result is diabetes mellitus.
Secondary diabetes mellitus can also occur in cats. This relates to insulin resistance rather than a reduction in the insulin produced, although both can be occurring at the same time. Some insulin resistance in cells may be due to genetic mutation causing a lower number of insulin receptors on the cell surface or structural defects in the receptor site. Other reasons are yet to be determined, although it is known that obese cats are more prone to it, as well as cats that have been receiving corticosteroids or are chronically stressed. Insulin resistance results in blood glucose levels remaining high, which stimulates increased insulin production until beta cell exhaustion decreases insulin secretion levels.
It is because these processes take a considerable amount of time that diabetes mellitus is usually seen in middle-aged and older cats. However, any disease that causes damage to the pancreas, such as an infection, may cause acute-onset (rapidly developing) diabetes mellitus in a cat of any age.
Clinical signs that can be seen in a cat with diabetes mellitus include:
* Polydipsia (increased water intake).
* Polyuria (increased urination).
* Polyphagia (increased food intake) combined with weight loss.
* Lethargy.
* Weakness.
* Plantigrade stance, the cat stands on his or her full foot rather than just the toes as is normal. This is due to nerve degradation from diabetic neuropathy. It is an uncommon complication, but cause for significant concern.
If your cat displays any or several of these clinical signs you should consult your veterinarian. If they start using a plantigrade stance, it would be best to take your pet to your veterinary clinic as quickly as possible.
For information on caring for and the treatment of a diabetic cat, please see the articles under Helium's title "How to care for a cat with diabetes."
Sources:
Adams, N. (2006) Unpublished Animal Physiology lectures.
Aroch, I, Mazaki-Tovi, M, Shemesh, O, Sarfaty, H & Segev, G. (2005) Central diabetes insipidus in five cats: clinical presentation, diagnosis and oral desmopressin therapy. Journal of Feline Medicine and Surgery 7(6): p333-339.
Cornell University College of Veterinary Medicine (2006) Feline diabetes.
http://www.vet.cornell.edu/fhc/resources/brochure/di abetes.html
Henson, M. & O'Brien, T. (2006) Feline models of type 2 diabetes mellitus. Institute of Laboratory Animal Resources 47(3): p234-242.
Kahn, C (Editor) (2006) The Merck Veterinary Manual. http://www.merckvetmanual.com/mvm/index.jsp
Nicholson, J. (2006) Unpublished Animal Disease lectures.
Randall, D., Burggren, W. & French, K. (2002) Eckert Animal Physiology Mechanisms and Adaptations 5th Edition. New York: W.H. Freeman & Company.
Taylor, S. (2001) Insulin action, insulin resistance and Type 2 Diabetes Mellitus.
http://books.mcgraw-hill.com/getommbid.php?template= ommbid&isbn=0071459960_68
University of Maryland Medical Center (2008) Diabetes insipidus nephrogenic.
http://www.umm.edu/ency/article/000511.htm
Walker, K. (2006) Unpublished Animal Disease lectures.
Walker, K. (2006) Unpublished Veterinary Immunology and Pharmacology lectures.