Effects of oral administration of orotic acid on hepatic morphologic characteristics and serum biochemical variables in cats

Jan L. VanSteenhouse From the Departments of Veterinary Pathology (VanSteenhouse, Taylor), Veterinary Clinical Sciences (Dimski, Taboada, Hosgood), and Veterinary Physiology, Pharmacology, and Toxicology (Swenson), School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803.

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Donna S. Dimski From the Departments of Veterinary Pathology (VanSteenhouse, Taylor), Veterinary Clinical Sciences (Dimski, Taboada, Hosgood), and Veterinary Physiology, Pharmacology, and Toxicology (Swenson), School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803.

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H. Wayne Taylor From the Departments of Veterinary Pathology (VanSteenhouse, Taylor), Veterinary Clinical Sciences (Dimski, Taboada, Hosgood), and Veterinary Physiology, Pharmacology, and Toxicology (Swenson), School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803.

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David H. Swenson From the Departments of Veterinary Pathology (VanSteenhouse, Taylor), Veterinary Clinical Sciences (Dimski, Taboada, Hosgood), and Veterinary Physiology, Pharmacology, and Toxicology (Swenson), School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803.

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Joseph Taboada From the Departments of Veterinary Pathology (VanSteenhouse, Taylor), Veterinary Clinical Sciences (Dimski, Taboada, Hosgood), and Veterinary Physiology, Pharmacology, and Toxicology (Swenson), School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803.

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Giselle Hosgood From the Departments of Veterinary Pathology (VanSteenhouse, Taylor), Veterinary Clinical Sciences (Dimski, Taboada, Hosgood), and Veterinary Physiology, Pharmacology, and Toxicology (Swenson), School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803.

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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)

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)

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