Life without lente or the glucose curve (Proceedings)


Life without lente or the glucose curve (Proceedings)

Aug 01, 2011


     • Discuss the etiology and progression of the diabetes in the cat
     • Compare and contrast the new insulins on the market
     • Discuss the pros and cons of the glucose curve, in-home monitoring and the use of fructosamine

Key points

     • The etiology of diabetes in cats is related to insulin resistance and glucose toxicity resulting in impairment of insulin secretion and beta cell destruction
     • Data supports the use of glargine in newly diagnosed diabetics to increase the chances of remission, i.e., reversing the need for insulin therapy
     • The newer insulins, such as lispro, aspart and detemir, have few studies in cats but have been used anecdotally in some cases
     • Dedicated owners may find home monitoring an attractive alternative when used in conjunction with monitoring of clinical signs and periodic fructosamine levels


Cats are true carnivores and as such have a metabolism specifically adapted to high protein meals:
     • Proteins (amino acids) provide the substrate for gluconeogenesis;
     • Cats continue to produce glucose even during the fed state;
     • Cats appear to be naturally "insulin resistant" as a means of maintaining euglycemia during long-periods of fasting that occur in the wild;
     • Cats have limited function of glucokinase, hexokinase and glycogen synthetase which are enzymes used to convert glucose to the glycogen.

These metabolic strategies mean that they are less efficient at "sopping up" post-prandial glucose loads that occur with high carbohydrate meals. Commercial dry diets, by virtue of the processing that must occur to create a dry diet, contain higher quantities of carbohydrates than the comparable canned diet. In order to deal with the post-prandial hyperglycemia, the pancreas secretes ever increasing levels of insulin, for a time, to maintain euglycemia. Obesity can add to the insulin resistance and stimulate additional insulin secretion. There are several problems with this scenario of hyperglycemia and initial hyperinsulinemia. With increased insulin secretion, there is increased amylin secretion, a molecule that is co-secreted with insulin. Amylin is then deposited back into the islet cells as amyloid causing destruction over time of the beta cell leading eventually to decreased insulin secretion. Hyperglycemia causes "glucose toxicity" in which glucose receptors on the beta cell become "desensitized" from chronic stimulation, thus impairing insulin secretion from the beta cell, again ultimately leading to decreased insulin secretion and exacerbation of hyperglycemia. This unique metabolism makes the cat predisposed to Type II diabetes given the twin evils of obesity and high carbohydrate diets. With on-going destruction of the beta cells, Type I diabetes can eventually occur.