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in Journal of the American Veterinary Medical Association
in Journal of the American Veterinary Medical Association

Abstract

Objective

To determine urinary orotic acid (OA) conentration and evaluate the urinary OA-to-creatinine ratio (OACR) in cats with hepatic lipidosis (HL).

Animals

20 cats with HL and 20 clinically normal cats.

Procedure

Hepatic lipidosis was diagnosed on the basis of clinical signs, results of serum biochemical analyses, exclusion of other concurrent illness, and cytologic or histologic evaluation of liver biopsy specimens. Urine samples were collected from each cat and frozen at −20 C until assayed. Urine creatinine concentrations were determined, using an alkaline picrate method followed by spectrophotometric assay. Urine OA concentration was determined, using high-performance liquid chromatography. Minimum amount of detectable OA in feline urine was 1 µg/ml. Because of small interfering peaks near the base of the OA peak, the minimum quantifiable concentration of OA was determined to be 5 pg/ml. Urinary OACR was compared in both groups of cats.

Results

Differences in urinary OACR were not detected between clinically normal cats and cats with HL. Peaks were not detected for urinary OA in any of the 20 clinically normal cats. Of the 20 HL cats, 14 did not have detectable peaks for urinary OA. Of the 6 HL cats that had detectable urinary OA peaks, 3 had values of < 5 µg/ml.

Conclusions

Apparently, OACR does not increase significantly in cats with HL.

Clinical Relevance

Urinary OACR is not a useful diagnostic test for HL in cats. (Am J Vet Res 1999; 60:753–754)

Free access
in American Journal of Veterinary Research

Abstract

Objective

To evaluate orotic acid (OA) as a possible etiologic factor in cats with idiopathic hepatic lipidosis (HL).

Animals

20 clinically normal adult female cats.

Procedure

Cats were fed a control diet or a diet containing less protein. On day 1 of the control period, blood, urine, and liver biopsy specimens were obtained. Each cat was given an oral dose of water daily. On days 8, 15, and 22, blood and urine specimens were collected as on day 1. On day 29, liver, blood, and urine samples were obtained as on day 1. After a resting period of 30 to 60 days, cats were treated with orotic acid. Serum biochemical analyses, urinary OA-to-creatinine ratios, and liver biopsy specimens were evaluated. Cats were given OA orally (suspension or capsules) for 29 days. Sample collection and data obtained were identical to those described for the control period.

Results

Urinary OA-to-creatinine ratios were significantly higher in all treated cats, but ratios were significantly higher in those receiving OA in capsules than in those receiving OA in suspension. Diet or treatment did not alter hepatic biochemical or histologic variables significantly. However, 7 cats given the highest dose of OA in capsules developed azotemia, urolithiasis, and renal changes.

Conclusions

Most concentrations of OA used in this study did not induce HL in cats during a 29-day period, but the highest dosage used did result in renal disease.

Clinical Relevance

Orotic acid does not appear to be involved in the genesis of HL in cats. (Am J Vet Res 1999;60:749–752)

Free access
in American Journal of Veterinary Research

Summary

Serum lipoprotein concentrations, routine serum biochemical values, and morphologic changes of the liver were evaluated in cats undergoing weight loss. Food was witheld from 6 obese and 6 control cats for 3 days (days 0 to 2), followed by feeding 50% of previous food intake for 26 days (days 3 to 28). Percutaneous liver biopsy specimens were obtained from all cats on days 0, 7, 14, and 28. Blood samples for serum biochemical analysis and lipoprotein profiles were obtained on days 0, 3, 7, 14, and 28. All cats lost weight throughout the study, and none developed signs of clinical illness, including those of idiopathic hepatic lipidosis syndrome. Serum total cholesterol concentrations decreased initially in all cats, but rapidly returned to normal after day 3 in obese cats, suggesting altered cholesterol metabolism during dietary restriction. Low-density lipoprotein concentrations decreased throughout the study in control cats, but were unchanged in obese cats. Examination of liver biopsy specimens from each cat revealed minimal lipid accumulation in all specimens, although some specimens contained hydropic degeneration.

Free access
in American Journal of Veterinary Research