Diabetes in Pets
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These methods may provide relief from glucose toxcicity suddenly and unexpectedly, risking overdose and [[hypoglycemia]] once the "glass floor" is broken. Caregivers should be vigilant about watching for signs that the floor has broken, such as lower than expected [[blood glucose level]]s or a [[rebound]] event on a previously "safe" insulin dosage, and be prepared to immediately lower the dosage.
 
These methods may provide relief from glucose toxcicity suddenly and unexpectedly, risking overdose and [[hypoglycemia]] once the "glass floor" is broken. Caregivers should be vigilant about watching for signs that the floor has broken, such as lower than expected [[blood glucose level]]s or a [[rebound]] event on a previously "safe" insulin dosage, and be prepared to immediately lower the dosage.
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In some animals there's a longer-term insulin resistance effect of glucose toxicity even after [[regulation]] is achieved -- this may show up as a gradual reduction of insulin requirements in a regulated animal, due to the gradual healing of formerly glucose-damaged tissue. This reduction in insulin requirements may or may not eventually lead to [[remission]].
   
 
See also the article on [[obstacles to regulation]].
 
See also the article on [[obstacles to regulation]].
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==External Links==
 
==External Links==
 
[http://www.jbc.org/cgi/content/full/279/41/42351 PNRI Journal Article on glucose toxicity including damage to pancreatic beta cells.]
 
[http://www.jbc.org/cgi/content/full/279/41/42351 PNRI Journal Article on glucose toxicity including damage to pancreatic beta cells.]
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[http://www.felinediabetes.com/phorum5/read.php?15,180387 Discussion of glucose toxicity on the FDMB]
   
 
[[Category:Conditions]][[Category:Complications]][[Category:Vicious circles]]
 
[[Category:Conditions]][[Category:Complications]][[Category:Vicious circles]]

Revision as of 12:48, 9 December 2005

Glucose toxicity refers to the oxidizing and hypertonic (dehydrating) properties of hyperglycemia, both of which continually stress and damage tissues in the body. But the term is also specifically used to refer to the phenomenon of temporary insulin resistance brought on by this tissue stress.

When a diabetic animal is hyperglycemic for long enough, the animal's damaged tissues may start having trouble using insulin. This in turn means that even a well-dosed animal may continue to have high blood sugar, leading to even more insulin resistance.

Various methods through this "glass floor" have been tried, to varying degrees of success. One way is to continue gradually raising insulin dosage until the tissues pick up the insulin and start absorbing glucose, then quickly back off to a lower dose. Another is to "jumpstart" the process with a fast-acting insulin or a deliberately high dose of the regular insulin, then quickly back off to a lower dose. Another is to reduce the carbohydrate content of the food further, or to eliminate dry food entirely (even low-carb dry food), thereby presenting less of an obstacle for insulin effectiveness and reducing insulin needs. Aggressive attempts to break glucose toxcicity are best regarded as dangerous and should be addressed in close partnership with a diabetes-experienced veterinarian.

These methods may provide relief from glucose toxcicity suddenly and unexpectedly, risking overdose and hypoglycemia once the "glass floor" is broken. Caregivers should be vigilant about watching for signs that the floor has broken, such as lower than expected blood glucose levels or a rebound event on a previously "safe" insulin dosage, and be prepared to immediately lower the dosage.

In some animals there's a longer-term insulin resistance effect of glucose toxicity even after regulation is achieved -- this may show up as a gradual reduction of insulin requirements in a regulated animal, due to the gradual healing of formerly glucose-damaged tissue. This reduction in insulin requirements may or may not eventually lead to remission.

See also the article on obstacles to regulation.

External Links

PNRI Journal Article on glucose toxicity including damage to pancreatic beta cells. Discussion of glucose toxicity on the FDMB