F igaro is a 14 year old spayed female DSH with a recent history of polyuria and polydipsia. Figaro's owner, tired of constantly cleaning up pee stains from her carpets, brings her to your clinic.
On physical examination, Figaro appears bright and alert with normal temperature, pulse, and respiration. She weighs approximately 10 pounds, has fairly clean teeth, and purrs when you pet her. You look in her chart to see her vaccination status; that's when you notice that she was weighed at 14 pounds just last year. You ask the owner how Figaro's appetite is and she replies "voracious." Eating well, but losing weight? Not a good sign.
You take a blood sample to check her serum glucose level, and express her bladder to take a urine sample. Glucose is supposed to be between 70-110 mg/dl; Figaro's is at 215. Constant eating, excessive drinking, constant urination, and a blood gluse level twice normal, coupled with weight loss means only one possible diagnosis.
This cat has mature-onset diabetes. Insulin levels have become inadequate for the body's needs. The actual serum concentration of circulating insulin may actually be normal, but it's low relative to the concentration of serum glucose.
This form of diabetes is not uncommon in older, obese cats. It is often caused by amyloidosis of the pancreatic islets (insular amyloidosis). The cause of the primary disease, amyloidosis itself is not well understood. Not all cats with insular amyloidosis have Type II diabetes and not all Type II diabetic cats show insular amyloidosis, but the two conditions are linked together and this case is an example of that linkage.
If insular amyloidosis is causing diabetes, it's because the islet b-cells are destroyed by pressure necrosis or lysis triggered by the deposition of the amyloid. A chronic inflammatory response may be present and the infiltration of the pancreas by lymphocytes and macrophages (with subsequent fibrosis) further contributes to destruction of the islets and the continued deposition of amyloid.
In early stage cases it may be possible to control the disease by dietary means. In this case, however, almost every b-cell has been destroyed by amyloid deposition so the amount of insulin available to the body is far too low to handle through dietary management. This is a case where control of the disease through insulin therapy may be the best route.
Deposition of amyloid can occur in other organs (kidney, heart, spleen) besides the pancreas, and cause disruptions of their functions, with subsequent organ failure and death often being the outcome.
In this composite image, you see the pancreas of a cat suffereing from this condition. The acinar regions of the exocrine pancreas are quite normal, but the normally cellular islets of Langerhans are obviously not. Where there would be cells there's nothing but an amorphous deposit of slightly eosinophilic matrix material.
The obliteration of the islets means they're unable to make insulin. As the disease progresses and the loss of islets continues, the condition grows worse because fewer and fewer beta cells are left. Eventually there is no insulin produced at all. Loss of insulin production leads to irreversible diabetes mellitus and the animal must be supported with exogenous insulin.
Since cells can't get glucose for ATP production they turn to other sources, especially proteins and fats. The wasting of flesh associated with untreated diabetes (this cat lost 29% of its original body weight in a year!) is due to breakdown of muscle proteins to get the amino acids as an energy source. Metabolism of fat and the breakdown of muscle in diabetics causes changes in blood pH, and also the elimination of ketone bodies in the urine.
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