Stress hyperglycemia in sick cats: a retrospective study over 4 years

Between January 1997 and December 2000 blood glucose concentrations were measured in 2278 sick cats at the time of their initial presentation at the hospital. In 827 cats (36%) hyperglycemia (blood glucose >8 mmol/l) was documented, 1388 cats (61%) had normal blood glucose levels, 63 cats (3%) were hypoglycemic. In 674 of 827 cats (81.5%) no further investigations were performed and the veterinarian judged the hyperglycemia to be stress related. In 153 of the 827 cats (18.5%) blood glucose measurements were repeated and/or serum fructosamine concentrations evaluated. In 106 cats (69%) stress hyperglycemia and in 47 (31%) diabetes mellitus was then diagnosed. Blood glucose concentrations in cats with stress hyperglycemia were between 8.1 and 60.4 mmol/l (Median 10.3), in cats with diabetes mellitus between 8.5 and 70.0 (Median 27.7). Blood glucose concentrations in cats with diabetes mellitus were significantly higher than in cats with stress hyperglycemia. Cats with stress hyperglycemia suffered from a variety of different diseases, the most frequently encountered were surgical problems, neoplasia, heart diseases, upper and lower urinary tract diseases. Blood glucose concentrations in cats with heart diseases and in cats with neoplasia was higher than in cats with other disorders, however, the difference was not significant. Cats with diabetes mellitus were significantly more frequent male castrated than cats with stress hyperglycemia. Cats with stress hyperglycemia were significantly older than cats with normoglycemia.     

Evaluation of a continuous glucose monitoring system in cats with diabetes mellitus

A continuous glucose monitoring system (CGMS) was evaluated in 14 cats with naturally occurring diabetes mellitus. The device measures interstitial fluid glucose continuously, by means of a sensor placed in the subcutaneous tissue. All cats tolerated the device well and a trace was obtained on 15/16 occasions. There was good correlation between the CGMS values and blood glucose concentration measured using a glucometer (r=0.932, P<0.01). Limitations to the use of the CGMS are its working glucose range of 2.2-22.2 mmol/l (40-400 mg/dl) and the need for calibration with a blood glucose measurement at least every 12 h. When compared to a traditional blood glucose curve, the CGMS is minimally invasive, reduces the number of venepunctures necessary to assess the kinetics of insulin therapy in a patient and provides a truly continuous glucose curve.     

Glucose lowering effects of inhaled insulin in healthy cats

Inhaled medications have proven effective and well tolerated in cats, and inhaled insulin has been used successfully for the management of diabetes mellitus in humans. Thus, we hypothesize that delivery of aerosolized regular insulin can lower blood glucose in healthy cats. Five adult cats were administered aerosolized 0.9% saline (IS), regular insulin intravenously (IV) 0.5 U/kg, and aerosolized regular insulin 15 U/kg (I15) and 25 U/kg (I25) and blood glucose was evaluated. Mean blood glucose was significantly lower at 15, 30 and 45 min in the I25 and IV groups compared to baseline. Similarly, the IV and I25 groups had a significantly greater maximal percent change in blood glucose than the IS group. Significantly more cats developed severe hypoglycemia (<50 mg/dl; 2.7 mmol/l) in the IV and I25 groups than in the IS group. Results of this study demonstrate that aerosolized insulin can effectively lower blood glucose concentrations in healthy cats.     

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

Medical records of 10 cats with transient clinical diabetes mellitus were reviewed. At the time diabetes was diagnosed, clinical signs included polyuria and polydipsia (10 cats), weight loss (8 cats), polyphagia (3 cats), lethargy (2 cats), and inappetence (1 cat). Mean (+/- SD) fasting blood glucose concentration was 454 +/- 121 mg/dL, mean blood glucose concentration during 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 serum insulin concentration was undetectable (6 cats) or within the reference range (4 cats) and serum insulin concentration did not increase after i.v. glucagon administration in any cat. Insulin-antagonistic drugs were being administered to 5 cats and concurrent disorders were identified in all cats. Management of diabetes included administration of glipizide (6 cats), insulin (3 cats), or both (1 cat), discontinuation of insulin-antagonistic drugs, and treatment of concurrent disorders. Insulin and glipizide treatment was discontinued 4-16 weeks (mean, 7 weeks) after the initial diagnosis of diabetes was confirmed. At the time treatment for diabetes was discontinued, clinical signs had resolved, mean fasting blood glucose concentration was 102 +/- 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 occurred in postglucagon serum insulin concentrations, insulin peak response, and total insulin secretion, compared with values obtained when clinical diabetes was diagnosed. Histologic abnormalities were identified in pancreatic islets of 5 cats in which pancreatic biopsies were obtained and included decreased number of islets (4 cats), islet amyloidosis (3 cats), and vacuolar degeneration of islet cells (3 cats). Mean beta cell density was significantly (P < .001) decreased in diabetic cats compared with control cats (1.4 +/- 0.7 versus 2.6 +/- 0.5%, respectively). Cells within islets stained positive for insulin, however, the number of insulin-staining cells per islet and the intensity of insulin staining were decreased in 5 and 2 cats, respectively. Clinical diabetes had not recurred in 1 cat after 6 years, in 4 cats lost to 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 diabetes recurred in 3 cats after 6 months, 14 months, and 3.4 years, respectively. These findings suggest that cats with transient clinical diabetes have pancreatic islet pathology, including decreased beta cell density, and that treatment of diabetes and concurrent disorders results in improved beta cell function, reestablishment of euglycemia, and a transition from a clinical to subclinical diabetic state.     

Serum fructosamine concentration in cats with overt hyperthyroidism.

OBJECTIVE: To determine the effect of hyperthyroidism on serum fructosamine concentration in cats. DESIGN: Cohort study. ANIMALS: 22 cats with overt hyperthyroidism. PROCEDURE: Hyperthyroidism was diagnosed on the basis of clinical signs, detection of a palpable thyroid gland, and high total serum thyroxine (T4) concentrations. Hyperthyroid cats with abnormal serum albumin, total protein, and glucose concentrations were excluded from the study. Samples for determination of serum fructosamine concentration were obtained prior to initiating treatment. Results were compared with fructosamine concentrations in healthy cats, cats in which diabetes had recently been diagnosed, and cats with hypoproteinemia. In 6 cats, follow-up measurements were obtained 2 and 6 weeks after initiating treatment with carbimazole. RESULTS: Serum fructosamine concentrations ranged from 154 to 267 mumol/L (median, 198 mumol/L) and were significantly lower than values in healthy cats. Eleven (50%) of the hyperthyroid cats had serum fructosamine concentrations less than the reference range. Serum fructosamine concentrations in hyperthyroid, normoproteinemic cats did not differ from values in hypoproteinemic cats. During treatment, an increase in serum fructosamine concentration was detected. CONCLUSIONS AND CLINICAL RELEVANCE: In hyperthyroid cats, concentration of serum fructosamine may be low because of accelerated protein turnover, independent of blood glucose concentration. Serum fructosamine concentrations should not be evaluated in cats with overt hyperthyroidism and diabetes mellitus. Additionally, concentration of serum fructosamine in hyperthyroid cats should not be used to differentiate between diabetes mellitus and transitory stress-related hyperglycemia.     

Rebound hyperglycemia following overdosing of insulin in cats with diabetes mellitus

Posthypoglycemic hyperglycemia (rebound hyperglycemia) after overdosing of insulin was diagnosed in 6 cats with diabetes mellitus. Administration of excessive insulin induced hypoglycemia within 4 to 8 hours, followed by rebound hyperglycemia. Diagnosis was made by serial blood glucose determinations during a 20- to 24-hour period after insulin administration. Four cats had a history of difficulty in regulating the diabetic state. In 2 cats, rebound hyperglycemia was diagnosed on routine serial blood glucose determinations. All of the cats were hyperglycemic for most of the day. Rebound hyperglycemia was observed with both intermediate (neutral protamine hagedorn) and long-acting (protamine zinc iletin) insulins, and the range of insulin doses at which the disorder developed overlapped previously determined therapeutic doses for these insulins in the cat. Urine glucose and single afternoon blood glucose determinations were inadequate and potentially misleading in monitoring diabetic cats receiving excessive amounts of insulin.     

Glycosylated Hemoglobin Concentration for Assessment of Glycemic Control in Diabetic Cats

Blood glycosylated hemoglobin (GHb) concentration was quantified in 84 healthy cats, 9 cats with stress-induced hyperglycemia, 37 cats with newly diagnosed diabetes mellitus, and 122 diabetic cats treated with insulin or glipizide. Diabetic control was classified as good or poor in insulin-treated or glipizide-treated cats based on review of history, physical examination findings, changes in body weight, and measurement of blood glucose concentrations. Blood GHb concentration was determined using an affinity chromatography assay. Mean blood GHb concentration was similar for healthy normoglycemic cats and cats with transient, stress-induced hyperglycemia, but was significantly (P < .001) higher in untreated diabetic cats when compared with healthy normoglycemic cats. Mean blood GHb concentration was significantly (P < .001) higher in 84 cats with poorly controlled diabetes mellitus when compared with 38 cats in which the disease was well controlled. Mean blood GHb concentration decreased significantly (P < .01) in 6 cats with untreated diabetes mellitus after insulin and dietary treatment. A similar significant (P < .01) decrease in mean blood GHb concentration occurred in 7 cats with poorly controlled diabetes mellitus after diabetic control was improved by an increase in insulin dosage from 1.1 ± 0.9 to 1.4 ± 0.6 U/kg/ 24 h and by feeding a diet containing increased fiber content and in 6 cats with transient diabetes mellitus 8.2 ± 0.6 weeks after discontinuing insulin treatment. There was a significant (P< .01) stress-induced increase in mean fasting blood glucose concentration and mean blood glucose concentration for 12 hours after administration of insulin or glipizide but no change in mean blood GHb concentration in 5 docile diabetic cats 12.2 ± 0.4 weeks after the cats became fractious as a result of frequent hospitalizations and blood samplings. Results of this study suggest that evaluation of blood GHb concentration may be a clinically useful tool for monitoring glycemic control of diabetes in cats.     

Serum fructosamine concentration in nondiabetic and diabetic cats

Differentiating transient hyperglycemia from diabetic hyperglycemia can be difficult in cats since single blood glucose measurements reflect only momentary glucose concentrations, and values may be elevated because of stress-induced hyperglycemia. Glycated protein measurements serve as monitors of longer-term glycemic control in human diabetics. Using an automated nitroblue tetrazolium assay, fructosamine concentration was measured in serum from 24 healthy control cats and 3 groups of hospitalized cats: 32 euglycemic, 19 transiently hyperglycemic, and 12 diabetic cats. Fructosamine concentrations ranged from 2.1 - 3.8 mmol/L in clinically healthy cats; 1.1 - 3.5 mmol/L in euglycemic cats; 2.0 - 4.1 mmol/L in transiently hyperglycemic cats; and 3.4 to >6.0 mmol/L in diabetic cats. Values for with-in-run precision at 2 fructosamine concentrations (2.64 mmol/L and 6.13 mmol/L) were 1.5% and 1.3%, respectively. Between-run coefficient of variation was 3.8% at a fructosamine concentration of 1.85 mmol/L. The mean fructosamine concentration for the diabetic group differed significantly (P=0.0001) from the mean concentrations of the other 3 groups. Poorly regulated or newly diagnosed diabetic cats tended to have the highest fructosamine values, whereas well-regulated or over-regulated diabetic cats had values approaching the reference range. As a single test for differentiating nondiabetic cats from diabetic cats, fructosamine was very sensitive (92%) and specific (96%), with a positive predictive value of 85% and a negative predictive value of 98%. Serum fructosamine concentration shows promise as an inexpensive, adjunct diagnostic tool for differentiating transiently hyperglycemic cats from poorly controlled diabetic cats.     

Diabetic cataracts: different incidence between dogs and cats

Diabetes mellitus is one of the most common endocrinopathies in the dog and cat. Diabetic cataract primarily affects the canine species and is rarely observed in the cat. It has been proposed that the incidence of cataracts in diabetic dogs is high because many of these patients have significant hyperglycemia despite insulin therapy. Age, gender, levels of serum glucose (before and during insulin therapy) and cataract formation were evaluated, retrospectively, in 23 dogs and 22 cats with diabetes mellitus. In the canine population, the groups with the highest frequency of presentation were females and sexually intact animals. In contrast, males and neutered animals were the most prevalent groups in the feline diabetic population. Over 80% of diabetic cats and dogs were older than 7 years. Our results confirm the almost total lack of cataracts in diabetic cats, while they were present in more than half of the dogs. A relation between the incidence of cataracts and the correspondent level of hyperglycemia in the canine and feline species could not be established. The estimation of the relative risk for the development of cataracts in diabetic dogs shows that some population groups have a higher probability for suffering from this ocular alteration. A relation between relative risk and the correspondent level of hyperglycemia in the various groups was not found. This fact indicates that other factors are involved in the unequal appearance of diabetic cataracts in dogs and cats.     

Insulin therapy in cats with diabetes mellitus

Thirteen cats with diabetes mellitus were evaluated. Clinical signs included polydipsia, polyuria, polyphagia, lethargy, and weight loss. Results of physical examination included obesity, hepatomegaly, mild seborrhea sicca, muscle wasting, and dehydration. One cat walked plantigrade and was suspected of having a diabetic neuropathy. Persistent hyperglycemia, glucosuria, high liver enzyme activities, hypercholesterolemia, hyperproteinemia, and low electrolyte concentrations were the common laboratory findings. In 3 cats diabetes mellitus developed after megestrol acetate therapy; 2 of these cats required only temporary insulin treatment. In a 3rd cat, which had no history of receiving diabetogenic drug therapy, remission of diabetes mellitus also was observed. Serum insulin and plasma glucose concentrations were determined in 6 cats after administration of an intermediate-acting insulin (isophane insulin) and in 3 cats after administration of a long-acting insulin (protamine zinc insulin). The insulin concentration peaked 2 to 6 hours after the injection of intermediate-acting insulin and 6 to 12 hours after the injection of long-acting insulin. The lowest glucose concentration was recorded 4 to 8 hours after injection of intermediate-acting insulin, and 6 to 12 hours after injection of long-acting insulin. It was concluded that, although insulin therapy must be adjusted to the individual, the diabetic cat usually requires twice-daily administration of isophane insulin; however, the protamine zinc insulin can be given once daily for satisfactory control.     

Xylazine-induced hyperglycemia in beef cattle.

Intravenous administration of xylazine to beef cattle (10 animals, 0.2 mg/kg of body weight) resulted in rapid onset (less than 15 minutes) of hyperglycemia. Plasma glucose values increased to 195 +/- 15 mg/dl and 305 +/- 10 mg/dl at 15 minutes and 3 hours, respectively. Concomitantly, plasma insulin concentrations dropped from 23 +/- 2 microU/ml before xylazine to 5.8 +/- 0.7 microU/ml and 2.4 +/- 0.3 microU/ml at 15 minutes and 3 hours, respectively. Parallel decreases (20%) were observed for percentage of hemoglobin, red blood cell number, and packed cell volume. Plasma urea nitrogen was significantly (P less than 0.01) incrased within 3 hours of xylazine administration (6.7 +/- 0.9 mg/dl vs 11.4 +/- 0.7 mg/dl). Marked changes in concentrations of plasma-free fatty acids were not observed. Alternative means of anesthesia must be considered in those instances in which biopsy material is to be used for studies of carbohydrate metabolism in vitro.     

Treatment of feline diabetes mellitus using an alpha-glucosidase inhibitor and a low-carbohydrate diet

The purpose of this study was to determine the effect of an alpha-glucosidase inhibitor (acarbose), combined with a low-carbohydrate diet on the treatment of naturally occurring diabetes mellitus in cats. Eighteen client-owned cats with naturally occurring diabetes mellitus were entered into the study. Dual-energy X-ray absorptiometry (DEXA) was performed prior to and 4 months after feeding the diet to determine total body composition, including lean body mass (LBM) and percent body fat. Each cat was fed a commercially available low-carbohydrate canned feline diet and received 12.5mg/cat acarbose orally every 12h with meals. All cats received subcutaneous insulin therapy except one cat in the study group that received glipizide (5mg BID PO). Monthly serum glucose and fructosamine concentrations were obtained, and were used to adjust insulin doses based on individual cat's requirements. Patients were later classified as responders (insulin was discontinued, n=11) and non-responders (continued to require insulin or glipizide, n=7). Responders were initially obese (>28% body fat) and non-responders had significantly less body fat than responders (<28% body fat). Serum fructosamine and glucose concentrations decreased significantly in both responder and non-responder groups over the course of 4 months of therapy. Better results were observed in responder cats, for which exogenous insulin therapy was discontinued, glycemic parameters improved, and body fat decreased. In non-responders, median insulin requirements decreased and glycemic parameters improved significantly, despite continued insulin dependence. The use of a low-carbohydrate diet with acarbose was an effective means of decreasing exogenous insulin dependence and improving glycemic control in a series of client-owned cats with naturally occurring diabetes mellitus.     

Serum Fructosamine Concentration as an Index of Glycemia in Cats With Diabetes Mellitus and Stress Hyperglycemia

The purpose of this study was to evaluate fructosamine concentrations in clinically healthy cats, sick cats with stress hyperglycemia, and untreated diabetic cats to determine the usefulness of this test in diagnosing diabetes mellitus in cats, and in differentiating the disease from stress-induced hyperglycemia. In addition, we evaluated if the degree of glycemic control in cats treated for diabetes influenced their serum fructosamine concentrations. In the 14 sick cats with stress hyperglycemia, the median serum fructosamine concentration (269 μmol/L) was not significantly different from the median value in the 26 clinically normal cats (252 μmol/L). Two of the 14 cats with stress hyperglycemia (14.3%) had serum fructosamine concentrations above the upper limit of the reference range (175 to 400 μmol/U; on the basis of these results, the test specificity was calculated as 0.86. In 30 cats with untreated diabetes mellitus, the median serum fructosamine concentration was 624 μmol/L, markedly higher than the value in either the normal cats or the cats with stress hyperglycemia. All but 2 of the 30 untreated diabetic cats (6.7%) had serum fructosamine concentration above the upper limit of the reference range; on the basis of these results, the sensitivity of serum fructosamine concentration as a diagnostic test for diabetes mellitus was 0.93. When 30 diabetic cats receiving treatment were divided into 3 groups according to their response to treatment (ie, poor, fair, and good), the 16 cats that had a good response to treatment had significantly lower serum concentrations of both glucose and fructosamine compared with cats that had either a fair or poor response to treatment. A significant correlation (r_s= .70, n = 100, P < .001) was found between serum concentrations of glucose and fructosamine. Results of this study indicate that quantification of serum fructosamine concentration is a meaningful test for the diagnosis of diabetes, for differentiating diabetes from stress hyperglycemia; and for monitoring the metabolic control in treated diabetic cats.     

Treatment of 46 cats with porcine lente insulin--a prospective, multicentre study

This prospective, multicentre, non-blinded, open study followed 46 cats with diabetes mellitus during treatment with porcine lente insulin (also known as porcine insulin zinc suspension, Caninsulin, Intervet) for 16+/-1 weeks (stabilization phase), with additional monitoring of some cats (n=23) for a variable period. At least three of the following were present at initial presentation: appropriate history of clinical signs consistent with diabetes mellitus, glucosuria, blood glucose greater than 15 mmol/l and fructosamine greater than 380 micromol/l. Insulin treatment was started at a dose rate of 0.25-0.5 IU/kg body weight twice daily, with a maximum starting dose of 2 IU/injection. Twenty-eight of the cats were classed as reaching clinical stability during the study, in 23 of these cats this was during the stabilization phase. Seven cats went into remission during the stabilization phase and one of the cats in week 56. Clinical signs of hypoglycaemia, significantly associated with a dose of 3 units or 0.5 IU/kg or more per cat (twice daily), were observed in nine of the 46 cats during the stabilization phase and concomitant biochemical hypoglycaemia was recorded in most cases. Biochemical hypoglycaemia, recorded in 6% of the blood glucose curves performed during the stabilization phase, was significantly associated with a dose rate of 0.75 IU/kg or more twice daily. This further highlights the need for cautious stepwise changes in insulin dose. The protocol used in the present study is suitable for and easy to use in practice. This study confirmed the efficacy and safety of porcine lente insulin (Caninsulin) in diabetic cats under field conditions.     

Basal glucosuria in cats

Objective of this study was to demonstrate the ubiquitous presence of glucose in urine of euglycemic cats by a highly sensitive glucose assay. The local electronic database was searched for results of quantitative urine glucose measurements in cats. A total of 325 feline urine glucose measurements were identified, of which 303 (93%) had been submitted by one of the co‐authors working in a near‐by small animal practice. After the exclusion of patients with kidney disease (n = 60), hyperthyroidism (n = 15), diabetes mellitus (n = 11), multiple diseases (n = 9) or steroid treatment (n = 3), as well as serial measurements (n = 87) and outliers (n = 8), the final study population consisted of 132 cats. Urine creatinine concentration was unavailable in five patients. Whereas all but one cat had glucose concentrations above the detection limit of the assay (0.11 mmol/L, Gluco‐quant Enzyme Kit/Roche Diagnostics), no positive glucose dipstick test result (Combur 9‐Test, Roche Diagnostics) was observed. The median (range) of urinary glucose concentration and the glucose‐to‐creatinine ratio (UGCR) was 0.389 (<0.11–1.665) mmol/L and 0.0258 (0.007–0.517) respectively. The UGCR was not affected by age, gender, breed or leukocyturia, whereas cats with hematuria had slightly higher values. Data show that so‐called “basal glucosuria” is present in the majority of cats and by no means diagnostic for diabetes mellitus or renal glucosuria. This has to be considered when using bio‐analytical methods with a low limit of quantification.     

Triglyceride response following an oral fat tolerance test in Burmese cats, other pedigree cats and domestic crossbred cats

Primary lipid disorders causing fasting triglyceridaemia have been documented infrequently in Burmese cats. Due to the known increased risk of diabetes mellitus and sporadic reports of lipid aqueous in this breed, the aim of this study was to determine whether healthy Burmese cats displayed a more pronounced pre- or post-prandial triglyceridaemia compared to other cats. Serum triglyceride (TG) concentrations were determined at baseline and variably at 2, 4 and 6h after ingestion of a high-fat meal (ie, an oral fat tolerance test) in a representative sample of Burmese and non-Burmese cats. The median 4 and 6h serum TG concentrations were significantly higher in Burmese cats (4h - 2.8mmol/l; 6h - 8.2mmol/l) than in other pedigree and domestic crossbred cats (4h - 1.5mmol/l; 6h - 1.0mmol/l). The non-Burmese group had post-prandial TG concentrations ranging from 0.6 to 3.9mmol/l. Seven Burmese cats had post-prandial TG concentrations between 6.6 and 19.0mmol/l, five had concentrations between 4.2 and 4.7mmol/l, while the remaining 15 had post-prandial concentrations between 0.5 and 2.8mmol/l. None of these Burmese cats had fasting triglyceridaemia. Most Burmese cats with a 4 h TG > 6.0 mmol/l had elevated fasting very low density lipoprotein (VLDL) concentrations. This study demonstrates that a proportion of Burmese cats in Australia have delayed TG clearance compared to other cats. The potential repercussions of this observation with reference to lipid aqueous, pancreatitis and diabetes mellitus in Burmese cats are discussed.     

Evaluation of plasma-ionized magnesium concentration in 122 dogs with diabetes mellitus: a retrospective study

The goal of this study was to evaluate plasma-ionized magnesium (iMg2+) concentration in a large group of dogs with naturally occurring diabetes mellitus and to determine whether dogs with diabetes mellitus have hypomagnesemia, as reported in diabetic humans and cats. Plasma iMg2+ concentrations were retrospectively evaluated at the time of initial examination of 122 diabetic dogs at the Matthew J. Ryan Veterinary Hospital of the University of Pennsylvania. Diabetic dogs were defined as having uncomplicated diabetes mellitus (DM, 78 dogs) diabetic ketoacidosis (DKA, 32 dogs), or ketotic nonacidotic diabetes mellitus (DK, 12 dogs) on the basis of presence or absence of metabolic acidosis or ketonuria. Twenty-two control dogs were used to determine reference values for plasma iMg2+ concentration in healthy dogs. Plasma iMg2+ concentration also was evaluated in 19 nondiabetic dogs with acute pancreatitis because many of the dogs with DKA had concurrent acute pancreatitis. Plasma iMg2+ concentration was significantly higher in dogs with DKA (median 0.41 mmol/L, reference range 0.14-0.72 mmol/L) than in dogs with DM (0.33 mmol/L, 0.17-0.65 mmol/L; P = .0002) or the control group (0.32 mmol/L, 0.26-0.41 mmol/L; P = .006). There were no significant differences between plasma iMg2+ concentrations in dogs with DM or DK compared with control dogs. We conclude that dogs with naturally occurring diabetes mellitus do not have marked hypomagnesemia on initial examination at a tertiary care center.     

Evaluation of serum fructosamine concentration as an index of blood glucose control in cats with diabetes mellitus.

Fructosamine, a glycated serum protein, was evaluated as an index of glycemic control in normal and diabetic cats. Fructosamine was determined manually by use of a modification of an automated method. The within-run precision was 2.4 to 3.2%, and the day-to-day precision was 2.7 to 3.1%. Fructosamine was found to be stable in serum samples stored for 1 week at 4 C and for 2 weeks at -20 C. The reference range for serum fructosamine concentration in 31 clinically normal colony cats was 2.19 to 3.47 mmol/L (mean, 2.83 +/- 0.32 mmol/L). In 27 samples from 16 cats with poorly controlled diabetes mellitus, the range for fructosamine concentration was 3.04 to 8.83 mmol/L (mean, 5.93 +/- 1.35 mmol/L). Fructosamine concentration was directly and highly correlated to blood glucose concentration. Fructosamine concentration also remained high in consort with increased blood glucose concentration in cats with poorly controlled diabetes mellitus over extended periods. It is concluded that measurement of serum fructosamine concentration can be a valuable adjunct to blood glucose monitoring to evaluate glycemic control in diabetic cats. The question of whether fructosamine can replace glucose for monitoring control of diabetes mellitus requires further study.     

High dose intravenous glucose tolerance test and serum insulin and glucagon levels in diabetic and non-diabetic cats: relationships to insular amyloidosis

The high dose intravenous glucose tolerance test and concurrent immunoreactive serum insulin and glucagon levels were measured and the results related to the presence or absence of pancreatic insular amyloid in 16 cats, seven of which were known to be diabetic. Control values for all parameters were established using seven additional clinicopathologically normal cats. Nine of the 16 cats had normal fasting blood glucose levels (less than 120 mg/dl) and impaired glucose tolerance. These cats had attenuated (3/9) or normal (6/9) 0 to 5 minute glucose-stimulated insulin secretion, rising 45 to 60 minute insulin secretion (7/9), low mean insulin/glucose ratio, and normal mean serum glucagon. Three of the nine cats with impaired glucose tolerance had insular amyloidosis. These three cats had significantly higher mean blood glucose levels during the glucose tolerance test than did cats with impaired glucose tolerance and no insular amyloid deposits. Also, these three cats accounted for three of the four longest glucose disappearance one-half times (T1/2S), three of the four lowest glucose disappearance coefficients, and three of the four lowest 0 to 5 minute insulin responses. The seven diabetic cats (fasting blood glucose levels greater than 120 mg/dl) had either low to low normal (6/7) or above normal (1/7) fasting insulin levels, no insulin response to intravenous glucose stimulation (6/7), and elevated mean serum glucagon levels. Insular amyloid was present in six of the seven diabetic cats. Three diabetic cats with marked insular amyloid deposits had glucose disappearance T1/2 and K (coefficient) values, serum insulin levels, serum glucagon levels, and insulin/glucose ratios which were not significantly different from the other three diabetic cats with slight to moderate insular amyloidosis. These results confirm a strong association between the occurrence, but not the extent of insular amyloidosis and diabetes mellitus in adult diabetic cats, although amyloid replacement of pancreatic islets does not appear to be the primary diabetogenic event. Rather, these results appear to be consistent with our hypothesis that insular amyloid deposition is a morphologic marker of primary B-cell dysfunction that is basic to the pathogenesis of the diabetic condition, and is reflected clinically by impaired glucose tolerance.     

Fructosamine concentrations in hyperglycemic cats.

The aims of this study were 1) to establish a reference range for fructosamine in cats using a commercial fructosamine kit; 2) to demonstrate that the fructosamine concentration is not increased by transient hyperglycemia of 90 min duration, simulating hyperglycemia of acute stress; and 3) to determine what percentage of blood samples submitted to a commercial laboratory from 95 sick cats had evidence of persistent hyperglycemia based on an elevated fructosamine concentration. Reference intervals for the serum fructosamine concentration were established in healthy, normoglycemic cats using a second generation kit designed for the measurement of the fructosamine concentration in humans. Transient hyperglycemia of 90 min duration was induced by IV glucose injection in healthy cats. Multisourced blood samples that were submitted to a commercial veterinary laboratory either as fluoride oxalated plasma or serum were used to determine the percentage of hyperglycemic cats having persistent hyperglycemia. The reference interval for the serum fructosamine concentration was 249 to 406 mumol/L. Transient hyperglycemia of 90 min duration did not increase the fructosamine concentration and there was no correlation between fructosamine and blood glucose. In contrast, the fructosamine concentration was correlated with the glucose concentration in sick hyper- and normoglycemic cats. It is concluded that the fructosamine concentration is a useful marker for the detection of persistent hyperglycemia and its differentiation from transient stress hyperglycemia. Fructosamine determinations should be considered when blood glucose is 12 to 20 mmol/L and only a single blood sample is available for analysis.