It is in many cases possible to induce remission (a temporary or permanent freedom from insulin-dependence) in diabetic cats. (This appears to be unique to cats, unfortunately for dogs and humans. Dogs may experience remissions if their diabetes has a transient or secondary cause.) There is growing agreement among experts[1][2] that a combination of low-carb healthy diet, well-chosen insulin, and well-chosen dosage plans can in many cases bring glucose levels and insulin requirements down to what the damaged pancreas can handle, and allow the cat's blood sugar to be controlled entirely by diet thereafter. (A low-carb diet is usually required for the remainder of the cat's life.)

Remission has been claimed (by Dr. Rand and Dr. Hodgkins) to be a realistic goal for all cats who can be properly regulated quickly. Chances of success are highest in the first few months after initial diagnosis. This limited time window is probably caused by amyloidosis and glucose toxicity, and is a good reason to start with low-carb diet and very slow-acting insulins, the most successful known combination, right away. Dr. Elizabeth Hodgkins[3] and Dr. Jacquie Rand[4] both recommend regimes of Tight regulation to achieve remission.

In cats whose diabetes has been recently caused by steroids or some other transient cause, remission seems particularly likely if regulation can be achieved early.

Note that Glipizide and similar oral diabetic medicines have been shown to increase amyloid production, and amyloidosis when blood sugar is high, damaging the pancreas and therefore making remission less likely.[5]

Insulin therapy for cats with "sputtering" pancreases

When a diabetic cat's pancreas begins again to produce insulin, that insulin production is seldom predictable or sufficient to immediately put the cat's blood glucose levels in a non-diabetic range. That is, a cat's recovering pancreas usually does not have a "full on" or "full off" switch. Achieving remission may take several weeks or months of careful monitoring and administration of insulin that is reduced in both timing and amount.

If a cat's pancreas is "sputtering," making the decision to administer exogenous insulin at all can be complicated. Some have referred to it as a game of "chicken." It is not unusual for a diabetic cat nearing remission to have a blood glucose level in the high 100s and for that level to fall, without exogenous insulin, to the low 100s or lower within a couple of hours. Adding exogenous insulin to the mix when that is happening could lead to hypoglycemic levels. In fact, unexpected falls of blood glucose levels to or near hypoglycemic levels on insulin dosages formerly known to be "safe" are a strong indicator of either more efficient use of insulin (healing glucose toxicity), or a sputtering, recovering pancreas.

In the first stage, insulin dosage may be gradually reduced to keep glucose levels in a safe range. This works until the cat begins producing enough endogenous insulin to be able to skip shots, even at the lowest possible doses. Then the next stage of attempted remission begins.

With a cat attempting remission, some caretakers choose a blood glucose level (be it 120 or 150 or 180) at or above which to administer exogenous insulin. The decision of whether to administer insulin in those situations should be affected by knowledge of when the cat last ate and whether the elevated level could be the result of food. Another consideration is the type of insulin being used, that is, whether it is a long-acting or fast-acting insulin. In these situations, even thorough knowledge of the cat's past reaction to various dosages of insulin may not provide sufficient information to make an appropriate dosing decision. You should carefully monitor a cat in this situation after an insulin injection to make sure it does not become hypoglycemic.

Research on cures

New research on possible cures for diabetes is starting to get promising, though the studies are currently in mice. Promising research includes:

  • Induced diabetic remission in mice by injecting donated spleen cells into the pancreas[6]
  • Induced diabetic remission in mice by deadening pain nerves in the pancreas[7]

Proposed Mechanism for Feline Diabetic Remission

Steve and Jock propose the following mechanism for remission in diabetic felines. This hypothesis relies on three premises:

1. Damaged feline pancreas can regenerate in 8-12 weeks, as livers are generally already accepted to do.

2. Hyperglycemia temporarily suppresses most insulin production in cats (as per Hodgkins and later also Rand[citation needed]).

3. Glucose toxicity plus amyloidosis permanently damage pancreatic beta cells[8]

If these three are all proven, then a mechanism suggests itself:

  • Beta cells are originally suppressed by some transient condition (such as high steroid dose, insulin resistance or overly high carbohydrate diet).
  • Consequent insulin shortage causes hyperglycemia, which by premise 2 suppresses beta cells and stops insulin production, keeping condition diabetic.
  • Glucose toxicity, by premise 3, damages pancreas, including newly regenerated cells, and prevents recovery.
  • Insulin therapy + low-carb diet keeps blood euglycemic for 24 hours out of 24 over a few days allowing insulin production to resume, though insulin resistance from damaged tissue remains.
  • Continuing euglycemia from insulin therapy and low-carb diet allows oxide-injured tissue to heal, reducing insulin resistance, leading to reduction in insulin dose.
  • Long-term euglycemia from Insulin therapy + low-carb diet over 8-12 weeks stops toxic oxidization of regenerating pancreatic cells, allowing more undamaged beta cells to produce insulin.
  • Required basal insulin supplementation drops to zero when newly-regenerated pancreas gradually reaches about 50% capacity, though bolus supplementation may still be needed in high-carb diet -- so no such diet should be attempted.
  • Pancreas, if unstressed by further blood sugar spikes, may continue to recover lost capacity as new cells regenerate.

Proving this mechanism might require studies to prove premise 1 and reinforce premise 2. Premise 3 is adequately shown, and the conclusion, that a low-carb diet plus careful slow-acting basal insulin supplementation, slowly decreased over 8-12 weeks, produces remission in more than half of newly-diagnosed cats, is shown by Rand & Marshall.

Note: According to Dr. Danielle Gunn-Moore and (she says) Dr. Jacquie Rand, these points "clearly describe the currently accepted hypothesis for DM remission in cats".

Case studies

See Category:Remission cases for stories of cats brought into remission.

Further Reading



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