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  • Author or Editor: Yasunori Ohba x
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Abstract

Objective—To evaluate postprandial changes in the leptin concentration of CSF in dogs during development of obesity.

Animals—4 male Beagles.

Procedures—Weight gain was induced and assessments were made when the dogs were in thin, optimal, and obese body conditions (BCs). The fat area at the level of the L3 vertebra was measured via computed tomography to assess the degree of obesity. Dogs were evaluated in fed and unfed states. Dogs in the fed state received food at 9 AM. Blood and CSF samples were collected at 8 AM, 4 PM, and 10 PM.

Results—Baseline CSF leptin concentrations in the thin, optimal, and obese dogs were 24.3 ± 2.7 pg/mL, 86.1 ± 14.7 pg/mL, and 116.2 ± 47.3 pg/mL, respectively. In the thin BC, CSF leptin concentration transiently increased at 4 PM. In the optimal BC, baseline CSF leptin concentration was maintained until 10 PM. In the obese BC, CSF leptin concentration increased from baseline value at 4 PM and 10 PM. Correlation between CSF leptin concentration and fat area was good at all time points. There was a significant negative correlation between the CSF leptin concentration–to–serum leptin concentration ratio and fat area at 4 PM; this correlation was not significant at 8 AM and 10 PM.

Conclusions and Clinical Relevance—Decreased transport of leptin at the blood-brain barrier may be 1 mechanism of leptin resistance in dogs. However, leptin resistance at the blood-brain barrier may not be important in development of obesity in dogs.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To investigate effects of short- and long- term administration of glucocorticoids, feeding status, and serum concentrations of insulin and cortisol on plasma leptin concentrations in dogs.

Animals—20 nonobese dogs.

Procedure—For experiment 1, plasma leptin concentrations and serum concentrations of insulin and cortisol were monitored for 24 hours in 4 dogs administered dexamethasone (0.1 mg/kg, IV) or saline (0.9% NaCl) solution for fed and nonfed conditions. For experiment 2, 11 dogs were administered prednisolone (1 mg/kg, PO, q 24 h for 56 days [7 dogs] and 2 mg/kg, PO, q 24 h for 28 days [4 dogs]) and 5 dogs served as control dogs. Plasma leptin and serum insulin concentrations were monitored weekly.

Results—For experiment 1, dexamethasone injection with the fed condition drastically increased plasma leptin concentrations. Furthermore, injection of saline solution with the fed condition increased plasma leptin concentrations. These increases in plasma leptin concentrations correlated with increases in serum insulin concentrations. Dexamethasone injection with the nonfed condition increased plasma leptin concentrations slightly but continuously. Injection of saline solution with the nonfed condition did not alter plasma leptin concentrations. For experiment 2, prednisolone administration at either dosage and duration did not alter plasma leptin concentrations in any dogs.

Conclusions and Clinical Relevance—Dexamethasone injection and feeding increased plasma leptin concentrations in dogs. In addition, dexamethasone administration enhanced the effect of feeding on increases in plasma leptin concentrations. Daily oral administration of prednisolone (1 or 2 mg/kg) did not affect plasma leptin concentrations in dogs.

Full access
in American Journal of Veterinary Research

Objective

To compare results of laboratory tests in dogs with vena caval syndrome before and after surgical removal of heartworms.

Design

Longitudinal uncontrolled clinical trial.

Animals

51 dogs with vena caval syndrome.

Procedure

Heartworms were removed from the area of the tricuspid valve and pulmonary arteries via venotomy and by use of flexible alligator forceps. Blood samples were obtained before and 10 days after removal of heartworms. Red and white blood cell counts were determined, using an automated cell counter. Biochemical tests were performed, using a dry chemical method.

Results

45 dogs survived the procedure, and 6 died or were euthanatized after surgical treatment. After surgery, RBC count and total protein, albumin, calcium, and sodium concentrations increased, and total bilirubin, ammonia, BUN, creatinine, uric acid, and potassium concentrations decreased in dogs that survived. Creatine kinase, L-lactate dehydrogenase, and amylase activities decreased, whereas alkaline phosphatase and ɣ-glutamyltransferase activities and total cholesterol concentration increased. Alanine transaminase activity decreased in 27 dogs but increased in 3 dogs. Changes in test results in dogs that did not survive were similar to those in dogs that did survive. Significant differences were found in RBC count, ɣ-glutamyltransferase activity, and total protein, total cholesterol, BUN, and total bilirubin concentrations before and after removal of heartworms.

Clinical Implications

Hepatic and renal functions improve rapidly after surgical removal of heartworms, presumably because general and pulmonary circulation is normalized. However, cholestasis may develop, and dogs that survive may need additional treatment to preserve hepatic function. (J Am Vet Med Assoc 1998;213:1134-1136)

Free access
in Journal of the American Veterinary Medical Association