Transient clinical diabetes mellitus in cats: 10 cases (1989-1991)

Medical records of 10 cats with transient clinical diabetes mellitus were r eviewed. Al the time diabetes was diagnosed, clinical signs included polyur ia and polydipsia (10 cats), weight loss (8 cats), polyphagia (3 cats): let hargy (2 cats), and inappetence (1 cat). Mean (+/-SD) fasting blood glucose concentration was 454 +/- 121 mg/dL, mean blood glucose concentration duri ng an 8-hour period (MBG/8 hours) was 378 +/- 72 mg/dL, and glycosuria and trace ketonuria were identified in 10 and 5 cats, respectively. Baseline se rum insulin concentration was undetectable (6 cats) or within the reference range (4 cars) and serum insulin concentration did nor increase after IV g lucagon administration in any cat. Insulin-antagonistic drugs were being ad ministered to 5 cats and concurrent disorders were identified in all cats. Management of diabetes included administration of glipizide (6 cats), insul in (3 cats), or both (1 cat), discontinuation of insulin-antagonistic drugs , and treatment of concurrent disorders. Insulin and glipizide treatment wa s discontinued 4-16 weeks (mean, 7 weeks) after the initial diagnosis of di abetes was confirmed. At the time treatment for diabetes was discontinued, clinical signs had resolved, mean fasting blood glucose concentration was 1 02 +/- 48 mg/dL, MBG/8 hours was 96 +/- 32 mg/dL, glycosuria and ketonuria were not identified in any cat, and concurrent disorders (except mild renal insufficiency in 1 cat) had resolved. Significant (P < .05) increases occu rred in postglucagon serum insulin concentrations, insulin peak response, a nd total insulin secretion, compared with values obtained when clinical dia betes was diagnosed. Histologic abnormalities were identified in pancreatic islets of 5 cats in which pancreatic biopsies were obtained and included d ecreased number of islets (4 cats), islet amyloidosis (3 cats), and vacuola r degeneration of islet cells (3 cats). Mean beta cell density was signific antly (P < .001) decreased in diabetic cats compared with control cats (1.4 +/- 0.7 versus 2.6 +/- 0.5%, respectively). Cells within islets stained po sitive for insulin, however, the number of insulin-staining cells per islet and the intensify of insulin staining were decreased in 5 and 2 cats, resp ectively Clinical diabetes had nor recurred in 1 cat after 6 years, in 4 ca ts lost ro follow-up after 1.5. 1.5, 2.0, and 2.5 years, and in 2 cats that died 6 months and 5.5 years after clinical diabetes resolved. Clinical dia betes recurred in 3 cats after 6 months, 14 months, and 3.4 years, respecti vely. These findings suggest that cats with transient clinical diabetes hav e pancreatic islet pathology, including decreased beta cell density, and th at treatment of diabetes and concurrent disorders results in improved beta cell function, reestablishment of euglycemia, and a transition from a clini cal to subclinical diabetic state.